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1
Bates, Amber, Carol Fischer, Vrushali Abhyankar, Georgia Johnson, Janet Guthmiller, Ann Progulske-Fox, and Kim Brogden. "Matrix Metalloproteinase Response of Dendritic Cell, Gingival Epithelial Keratinocyte, and T-Cell Transwell Co-Cultures Treated with Porphyromonas gingivalis Hemagglutinin-B." International Journal of Molecular Sciences 19, no. 12 (December 7, 2018): 3923. http://dx.doi.org/10.3390/ijms19123923.
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Matrix metalloproteinases (MMPs) are enzymes involved in periodontal tissue destruction. Hemagglutinin B (HagB) from the periodontal pathogen Porphyromonas gingivalis induces an elevated MMP response in dendritic cells, but responses from cultures of single-cell types do not reflect the local tissue environment. The objective of this study was to measure HagB-induced MMP responses in a transwell co-culture system containing dendritic cells, gingival epithelial (GE) keratinocytes, and CD4+ T-cells. Transwell co-cultures were assembled and treated with or without HagB. Immunoassays were used to determine production of MMP1, MMP7, MMP9, and MMP12 in response to HagB up to 64 h. Control responses were subtracted from HagB-induced responses. A two-way fixed effect ANOVA was fit to log-transformed concentrations and pairwise group comparisons were conducted (p < 0.05). At 64 h, dendritic cells produced elevated MMP1 and MMP9 responses, which were attenuated in the 3-cell co-culture (p < 0.05). There were also significant differences in MMP7 and MMP12 production between single-cell cultures and co-cultures. These results support the need to use multiple cell types in culture models to evaluate a more representative response to proinflammatory agonists. This three-cell transwell co-culture model may help us better understand the inflammatory process in periodontal disease and test novel therapeutic approaches.
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Hua, Li, and Han Zhengxue. "The chemotaxis study of adipose derived stem cells (ADSCs) to adenoid cystic carcinoma (ACC) cells." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e17000-e17000. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e17000.
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e17000 Background: Adenoid cystic carcinoma (ACC) has some properties such as neurotropic, angiotropic and early metastasis, recurrence and metastasis is the leading cause of poor prognosis in sACC. The current theory is that the invasion and metastasis were related to tumor stem cells, and the stem cell microenvironment play an important role in this process. According to the stem cell theory, we hypothesized that normal tissue stem cells may also produce chemotactic migration to tumor stem cell microenvironment, therefore this research was to explore the possibility of adipose derived stem cells as a therapy vector targeted to the microenvironment of ACC. Methods: Conventionally culture ACC cells to logarithmic growth phase, then collected them and cultured in serum-free medium. After 48 h, the culture supernatant was collected, filtered and prewarmed, and then added to each well (24-well plate, the lower chamber of the transwell chamber), 600-800 ul for each. Using the same method, the culture supernatant of T293 cells were joined into the lower chamber as a control. Then, the transwell membrane was gently placed into the well, and 100 ~ 150μl suspension of adipose derived stem cells in the logarithmic growth phase (serum-free media) were added into the upper chamber. After cultured under routine conditions for 24 hours, the transwell chamber were removed , fixed and stained. Under bright field microscope, cells invasived and attached to the transwell membrane were observed and counted, results were statistically analyzed by student test. Results: Selecte five high-power microscopic field randomly, counted the number of adipose derived stem cells migrated to transwell membrane of different cell lines. Results showed that migrated cell number of SACC-LM group was 64.3 ± 7.6, the number of SACC-83 group was 52.3 ± 6.1, both higher than the T293 group (31.8 ± 6.3), and the difference between them was statistically significant (p <0.05). Conclusions: Adipose derived stem cells have obvious chemotaxis to adenoid cystic carcinoma cell culture supernatants, so we can propose that adipose derived stem cells has the possibility and feasibiliy of being used as a targeted therapy vectors for ACC.
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Xu, Gang, Lihua Zhu, Yan Wang, Yawei Shi, Aihua Gong, and Chaoyang Wu. "Stattic Enhances Radiosensitivity and Reduces Radio-Induced Migration and Invasion in HCC Cell Lines through an Apoptosis Pathway." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/1832494.
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Purpose. Signal transducer and activator of transcription factor 3 (STAT3) is involved in tumorigenesis, development, and radioresistance of many solid tumors. The aim of this study is to investigate the effects of stattic (an inhibitor of STAT3) on the radiosensitivity and radio-induced migration and invasion ability in hepatocellular carcinoma (HCC) cell lines. Methods. HCC cells were treated with stattic, and cell survival rate was analyzed through CCK-8 assay. Radiosensitivity was evaluated using cloning formation analysis; STAT3, p-STAT3, and apoptosis related proteins were detected by western blot. Radio-induced migration and invasion ability in HCC cells were analyzed by wound-healing assay and transwell test. Results. Stattic inhibits the expression of p-STAT3 and reduces cell survival in a dose-dependent manner in HCC cell lines, and the IC50 values for Hep G2, Bel-7402, and SMMC-7721 are 2.94 μM, 2.5 μM, and 5.1 μM, respectively. Cloning formation analysis shows that stattic enhances the radiosensitivity of HCC cells. Wound-healing assay and transwell test show that stattic inhibits radio-induced migration and invasion. Further study indicates that stattic promotes radio-induce apoptosis through regulating the expression of apoptosis related proteins in HCC cells. Conclusion. Stattic enhances radiosensitivity and reduces radio-induced migration and invasion ability in HCC cells probably through apoptosis pathway.
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Liu, Bing, Lili Xu, Xinming Yu, Xuefei Jiao, Junwei Yan, Wei Li, and Mingjin Guo. "Genistein Inhibited Estradiol-Induced Vascular Endothelial Cell Injury by Downregulating the FAK/Focal Adhesion Pathway." Cellular Physiology and Biochemistry 49, no. 6 (2018): 2277–92. http://dx.doi.org/10.1159/000493830.
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Background/Aims: In this study, we aimed to investigate the effects of genistein on the focal adhesion signaling pathway through its regulation of FAK. Genistein ultimately restored and alleviated estradiol-induced vascular endothelial injury. Methods: Microarray analysis was used to select differentially expressed genes. MTT assay was performed to detect the cell activity, and ROS test and NO test were performed to detect the degree of damage to HUVECs (human umbilical vein endothelial cells). The relative mRNA expression levels and protein expression levels of FAK were tested by western blot and qRT-PCR. GO functional analysis and KEGG pathway analysis were applied to predict the possible relationship between functions and related pathways, and transwell assay was used to detect cell invasion and migration. Results: FAK was highly expressed in the HUVECs treated with estradiol (HU-ESTs). Cell viability and NO level decreased, whereas ROS level increased in the HU-ESTs. Effective knockdown of FAK in HU-ESTs elevated cell viability and NO levels while suppressing ROS levels. In addition, inhibition of FAK greatly decreased cell invasion and migration, while the overexpression of FAK enhanced cell invasion and migration. KEGG further indicated focal adhesion pathways were activated. Genistein elevated HU-EST viability, and NO and ROS level increased in a concentration dependent manner. Transwell and western blot assays revealed that genistein could reduce the FAK expression levels and alleviate the damage to the HU-ESTs. Conclusion: FAK overexpression promoted invasion and migration of the HU-ESTs. However, genistein greatly suppressed FAK and estradiol-induced vascular endothelial cell injury.
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Zhou, Yunfei, Changqin Zhang, Qidong Zhang, Li Zhang, and Wenhu Liu. "Original article. The role of p38MAPK in asymmetric dimethylarginineinduced cytoskeleton and cellular permeability changes in cultured endothelial cells." Asian Biomedicine 5, no. 4 (August 1, 2011): 449–57. http://dx.doi.org/10.5372/1905-7415.0504.059.
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Abstract Background: Asymmetric dimethylarginine (ADMA) induces endothelial cell barrier dysfunction via cytoskeleton activation and contraction. It is supposed that activated p38 mitogen-activated protein kinase (MAPK) would trigger the formation of stress fibers and increase cellular permeability. Objective: Explore p38 MAPK as a potentially important enzyme in ADMA-mediated endothelial cell contractile response and permeability change. Methods: Human umbilical endothelial cells (HUVECs) were cultured, where ADMA and/or SB203580 (the specific inhibitor of p38MAPK) were used to stimulate HUVECs. Immunofluorescent staining was carried out to examine the expression and distribution of F-actin, flow cytometry was used to quantify F-actin, and Transwell was applied to test cellular permeability with FITC-labelled human serum albumin (HSA). Scanning electronic microscopy (SEM) was utilized to observe the changes of intercellar contact. Results: ADMA induced significant p38MAPK activation in a dose-dependent manner, which correlated with increased stress fibers. SB-203580 attenuated the formation of actin stress fiber and the increase of cellular permeability induced ADMA in the HUVECs (p<0.01, LSCM; p<0.01, cytometry; p<0.05, Transwell). Widened intercellular space induced by ADMA was detected and could be inhibited by SB-203580 (SEM). SB-203580 alone had no effect on cytoskeleton and cellular permeability. Conclusion: p38MAPK activation participated in cytoskeleton and cellular permeability changes induced by ADMA in HUVECs.
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Zhang, Zhenyu, Yan Wang, Mingchao Li, Jiaping Li, and Jian Wu. "Fibroblast Growth Factor 18 Increases the Trophic Effects of Bone Marrow Mesenchymal Stem Cells on Chondrocytes Isolated from Late Stage Osteoarthritic Patients." Stem Cells International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/125683.
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Coculture of mesenchymal stem cells with chondrocytes increases production of cartilaginous matrix. Chondrocytes isolated from late stage osteoarthritic patients usually lost their phenotype of producing cartilaginous matrix. Fibroblast growth factor 18 is believed to redifferentiate OA chondrocyte into functionally active chondrocytes. The aim of this study is to investigate the supportive effects of MSCs on OA chondrocytes and test if FGF18 could enhance the responsiveness of OA chondrocytes to the support of MSCs in a coculture system. Both pellet and transwell co-cultures were used. GAG quantification, hydroxyproline assay, and qPCR were performed. An ectopic models of cartilage formation was also applied. Our data indicated that, in pellets coculture of MSCs and OA chondrocytes, matrix production was increased in the presence of FGF18, comparing to the monoculture of chondrocytes. Results from transwell coculture study showed that expression of matrix producing genes in OA chondrocytes increased when cocultured with MSCs with FGF18 in culture medium, while hypertrophic genes were not changed by coculture. Finally, coimplantation of MSCs with OA chondrocytes produces more matrix than chondrocytes only. In conclusion, FGF18 can restore the responsiveness of OA chondrocytes to the trophic effects of MSCs. Coimplantation of MSCs and OA chondrocytes treated with FGF18 may be a good alternative cell source for regenerating cartilage tissue that is degraded during OA pathological changes.
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Zhang, Mingjuan, Huaming Deng, Xiajun Yi, Siying Xie, and Qingying Zhan. "Study on Chlorogenic Acid Inhibiting the Proliferation and Invasion of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis Model." Journal of Biomaterials and Tissue Engineering 11, no. 11 (November 1, 2021): 2192–96. http://dx.doi.org/10.1166/jbt.2021.2797.
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This paper explored Chlorogenic acid regulating the biological behavior of RA FLSs and studied the functional role of microRNAs in it. In vivo experiment: Female DBA/1 J mice were used for model establishment and grouping. HE staining was employed. The damage of ankle cartilage was analyzed in each group of mice. The levels of serum cytokines TNF-α and IL-β were measured by ELISA. In vitro experiment: The cells were counterstained with Hoechst 33342, Transwell was used to detect cell invasion. Western blotting was used to detect the expression of Akt protein. The Akt expression plasmid and miR-23b mimic were co-transfected into RA FLSs, and the luciferase activity was measured using a dual-luciferase detection system. In vivo experiments found that Chlorogenic acid can significantly reduce arthritis index and inhibit TNF-α and IL-β levels. In vitro experiments found that TNF-α-induced proliferation of RA FLSs was significantly inhibited by Chlorogenic acid. Transwell invasion test showed that TNF-α-induced cell invasion was attenuated at the presence of Chlorogenic acid, which significantly inhibited Akt protein expression and phosphorylation. The expression of miR-23b in Chlorogenic acid-treated RA-FLSs increased, and silencing miR-23b enhanced the inhibitory effect of RA FLSs on Chlorogenic acid induction. Chlorogenic acid has potential anti-rheumatoid arthritis activity. Its inhibition of RA FLSs proliferation and invasion is related to the induction of miR-23b and the down-regulation of Akt expression.
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Amini, Elham, Abhinav Kurumaddali, Sharvari Bhagwat, Simon M. Berger, and Günther Hochhaus. "Optimization of the Transwell® System for Assessing the Dissolution Behavior of Orally Inhaled Drug Products through In Vitro and In Silico Approaches." Pharmaceutics 13, no. 8 (July 21, 2021): 1109. http://dx.doi.org/10.3390/pharmaceutics13081109.
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The aim of this study was to further evaluate and optimize the Transwell® system for assessing the dissolution behavior of orally inhaled drug products (OIDPs), using fluticasone propionate as a model drug. Sample preparation involved the collection of a relevant inhalable dose fraction through an anatomical mouth/throat model, resulting in a more uniform presentation of drug particles during the subsequent dissolution test. The method differed from previously published procedures by (1) using a 0.4 µm polycarbonate (PC) membrane, (2) stirring the receptor compartment, and (3) placing the drug-containing side of the filter paper face downwards, towards the PC membrane. A model developed in silico, paired with the results of in vitro studies, suggested that a dissolution medium providing a solubility of about 5 µg/mL would be a good starting point for the method’s development, resulting in mean transfer times that were about 10 times longer than those of a solution. Furthermore, the model suggested that larger donor/receptor and sampling volumes (3, 3.3 and 2 mL, respectively) will significantly reduce the so-called “mass effect”. The outcomes of this study shed further light on the impact of experimental conditions on the complex interplay of dissolution and diffusion within a volume-limited system, under non-sink conditions.
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Liang, Jianwei, Teng Sun, Guoxiang Wang, and Hao Zhang. "Clinical significance and functions of miR-203a-3p/AVL9 axis in human non-small-cell lung cancer." Personalized Medicine 17, no. 4 (July 1, 2020): 271–82. http://dx.doi.org/10.2217/pme-2019-0108.
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Aim: We aimed to investigate the clinical significance and biological function of miR-203a-3p in non-small-cell lung cancer (NSCLC). Methods: The association between miR-203a-3p expression and clinicopathological parameters in NSCLC was assessed by χ2 test. Kaplan–Meier method and Cox regression model were applied to evaluate the prognosis value of miR-203a-3p. The biological function of miR-203-3p was explored using CCK-8 and transwell assays. Results: Significantly downregulated miR-203a-3p was associated with TNM stage, lymph node metastasis and poor prognosis. AVL9 was identified as a direct target of miR-203a-3p. Functionally, we found overexpression of miR-203a-3p inhibited cell proliferation, migration and invasion in NSCLC cells by targeting AVL9. Conclusion: Collectively, targeting the miR-203a-3p/ AVL9 axis might help to develop useful therapeutic target for NSCLC.
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Zheng, Jianxing, Daming Cheng, Dongyang Wu, Libing Wang, Fengzhi Qu, Xiaotang Wu, Ling Cheng, Yanbin Wei, and Xiaogang Liu. "MiR-452-5p mediates the proliferation, migration and invasion of hepatocellular carcinoma cells via targeting COLEC10." Personalized Medicine 18, no. 2 (March 2021): 97–106. http://dx.doi.org/10.2217/pme-2020-0027.
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Objective: This study explored the potential function of miR-452-5p in hepatocellular carcinoma (HCC) and clarified the mechanism underlying HCC progression. Materials & methods: Real-time quantitative PCR was used to detect miR-452-5p and COLEC10 mRNA expression in HCC, western blot was performed to test COLEC10 protein expression. The regulatory mechanism of miR-452-5p/COLEC10 in HCC cells was explored using CCK-8, wound healing assay, Transwell and dual-luciferase reporter assay. Results: MiR-452-5p was greatly upregulated in HCC cells, and it served as an oncogene playing an active role in HCC cell proliferation, migration and invasion. COLEC10 was identified as the target of miR-452-5p in HCC attenuating the promoting effect of miR-452-5p on HCC cells upon overexpression. Conclusion: MiR-452-5p can promote the progression of HCC via targeting COLEC10.
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De Simone, Uliana, Francesca Caloni, Laura Gribaldo, and Teresa Coccini. "Human Co-culture Model of Neurons and Astrocytes to Test Acute Cytotoxicity of Neurotoxic Compounds." International Journal of Toxicology 36, no. 6 (November 2017): 463–77. http://dx.doi.org/10.1177/1091581817739428.
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Alternative methods and their use in planning and conducting toxicology experiments have become essential for modern toxicologists, thus reducing or replacing living animals. Although in vitro human co-culture models allow the establishment of biologically relevant cell–cell interactions that recapitulate the tissue microenvironment and better mimic its physiology, the number of publications is limited specifically addressing this scientific area and utilizing this test method which could provide an additional valuable model in toxicological studies. In the present study, an in vitro model based on central nervous system (CNS) cell co-cultures was implemented using a transwell system combining human neuronal cells (SH-SY5Y cell line) and glial cells, namely astrocytes (D384 cell line), to investigate neuroprotection of D384 on SH-SY5Y and vice versa. The model was applied to test acute (24-48 hours) cytotoxicity of 3 different neurotoxicants: (1) methyl mercury (1-2.5 μM), (2) Fe3O4 nanoparticles (1-100 μg/mL), and (3) methylglyoxal (0.5-1 mM). Data were compared to mono-cultures evaluating the mitochondrial function and cell morphology. The results clearly showed that all compounds tested affected the mitochondrial activity and cell morphology in both mono-culture and co-culture conditions. However, astrocytes, when cultured together with neurons, diminish the neurotoxicant-induced cytotoxic effects that occurred in neurons cultured alone, and astrocytes become more resistant in the presence of neurons. This human CNS co-culture system seems a suitable cell model to feed high-throughput acute screening platforms and to evaluate both human neuronal and astrocytic toxicity and neuroprotective effects of new and emerging materials (eg, nanomaterials) and new products with improved sensitivity due to the functional neuron–astrocyte metabolic interactions.
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Zeng, Yi, Karl Staser, Keshav Mohan Menon, Su-jung Park, Muithi Mwanthi, Li Jiang, and D. Wade Clapp. "Ezrin Regulates Hematopoietic Stem/Progenitor Cell Motility." Blood 118, no. 21 (November 18, 2011): 1282. http://dx.doi.org/10.1182/blood.v118.21.1282.1282.
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Abstract Abstract 1282 Ezrin is a member of the ERM (ezrin, moesin and radixin) protein family that links plasma membrane proteins to the actin cytoskeleton. Ezrin in other in vitro cell systems has been hypothesized to participate in cell-cell contact and could have a role in stem/ progenitor cell mobilization and adhesion. To test this hypothesis, we crossed ezrinflox/flox mice with Mx1 cre transgenic mice to generate an inducible ezrin knock out mouse model. Inducible disruption of the ezrin gene in hematopoietic cells was achieved by the administration of polyIC. Ezrin knock out HSPCs exhibited a 30–40% decrease in baseline and chemokine stromal cell-derived factor-1 (SDF-1) stimulated motility in transwell migration assays in vitro. In addition, loss of ezrin led to a 60% decrease in the homing capacity of HSPCs in lethally irradiated recipient mice following transplantation. There was a 40–55% decrease in colony forming cells in peripheral blood and spleen of the mice following ezrin knock out, suggesting that ezrin knock out HSPCs may be deficient in egressing out of the bone marrow. To further understand the cause of the impaired motility of ezrin knock out HSPCs, we examined F-actin level of HSPCs at baseline and in response to SDF-1. Ezrin knock out HSPCs displayed 1.5 to 2 fold higher level of F-actin at baseline when compared with wild type cells. Following stimulation with SDF-1, wild type HSPCs that migrated to the bottom compartment of the transwell demonstrated a 2 time greater decrease in F-actin level when compared with ezrin knock out cells, suggesting that ezrin may participate in the regulation of F-actin depolymerization in HSPCs. In summary, we demonstrate that ezrin modulates HSPC migration and homing likely through its regulation on F-actin organization. Disclosures: No relevant conflicts of interest to declare.
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Zhang, Fan, Changsong Wang, Yinghua Cui, Shuping Li, Yuanfei Yao, Yanpeng Ci, Jinghe Wang, Wei Hou, Anqi Wu, and Enyou Li. "Effects of Propofol on Several Membrane Characteristics of Cervical Cancer Cell Lines." Cellular Physiology and Biochemistry 40, no. 1-2 (2016): 172–82. http://dx.doi.org/10.1159/000452535.
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Background: Although significant advances have been made toward understanding the molecular mechanisms underlying the effect of propofol on tumor cell metastasis, less is known regarding how cell membrane and cytoskeletal ultrastructure are affected in this process. Here, we investigated the relationship between cell morphology and cell size, which are features mainly defined by the cytoskeleton. Methods: To confirm the effects of propofol on the migratory ability of human cervical carcinoma cells, cell migration and invasion were examined through scratch wound healing and transwell membrane assays. Furthermore, HeLa cells cultivated with different concentrations of propofol were examined by confocal microscopy and atomic force microscopy (AFM), and the mean optical density and migration ability of these cells were also assessed. In addition, cell membrane morphology was inspected using AFM. Results: The results of the wound healing and transwell membrane assays indicated that propofol decreases the migratory ability of cervical carcinoma cells compared to control cells. A comparative analysis of the test results revealed that short-term (3 h) exposure to propofol induced marked changes in cell membrane microstructure and in the cytoskeleton in a dose-dependent manner. These morphological changes in the cell membrane were accompanied by cytoskeleton (F-actin) derangement. The present findings demonstrate a close relationship between changes in cell membrane ultrastructure and cytoskeletal alterations (F-actin) in propofol-treated HeLa cells. AFM scanning analysis showed that cell membrane ultrastructure was significantly changed, including a clear reduction in membrane roughness. Conclusion: The influence of propofol on the HeLa cell cytoskeleton can be directly reflected by changes in cellular morphology, as assessed by AFM. Moreover, the use of AFM is a good method for investigating propofol-mediated changes within cytoskeletal ultrastructure.
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Gao, Hong, Peipei Tang, Kejie Ni, Lun Zhu, Song Chen, Yulong Zheng, and Yufeng Wan. "Inhibition of Kelch-like epichlorohydrin-related protein 1 promotes the progression and drug resistance of lung adenocarcinoma." PeerJ 9 (August 19, 2021): e11908. http://dx.doi.org/10.7717/peerj.11908.
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Background Lung cancer is a common malignant carcinoma of respiratory system with high morbidity and mortality. Kelch-like epichlorohydrin-related protein 1 (Keap1), a member of the BTB-Kelch protein family, has been reported as an important molecule in several cancers. However, its potential role in tumor is still controversial. Here we aim to clarify the effect of Keap1 on the biological characteristics and chemotherapy resistance in lung adenocarcinoma (LUAD). Methods Immunohistochemistry was conducted to compare Keap1 expression in lung adenocarcinoma tissues and matched non-cancerous tissues, and the correlation between Keap1 expression and clinicopathological features was analyzed. Subsequently, the stable A549 and H1299 cell lines with Keap1 knockdown or overexpression were constructed using lentivirus. The roles of Keap1 on the cell proliferation, migration, invasion and drug resistance were investigated by colony formation assay, cell proliferation assay, wound scratch test, transwell invasion assay and drug sensitivity assay, respectively. Results Keap1 was lowly expressed in tumor tissues compared to matched non-cancerous tissues, and its expression was correlated with TNM stage and lymph node metastasis. Early stage (I) tumors without lymph node metastasis had higher levels of Keap1 expression compared with late-stage tumors (II, III) with the presence of lymphatic metastasis. Colony formation assays showed that Keap1 knockdown promoted the proliferation of A549 and H1299 cells, and the cell growth curves further confirmed this feature. In contrast, wound scratch and transwell invasion experiments showed that Keap1 overexpression inhibited cell migration and invasive malignancy. The IC50 for cisplatin and paclitaxel were significantly increased by Keap1 knockdown in A549 and H1299 cell lines. Conclusion Keap1 knockdown promotes tumor cell growth, proliferation, invasion, metastasis and chemotherapy resistance in LUAD. It may be a potential tumor marker to guide the staging and treatment of lung cancer.
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Yu, Chunrui, Aihua Zhang, and Hong Liu. "miRNA-122a as a Biomarkers in Prostatic Cancer." Journal of Biomaterials and Tissue Engineering 9, no. 12 (December 1, 2019): 1693–98. http://dx.doi.org/10.1166/jbt.2019.2203.
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Aim: The purpose of our work was to evaluate the correlation between miRNA-122a and diagnosis and treatment of prostatic cancer. Methods : The 30 tumor and normal tissues were collected from prostatic cancer cases, evaluated miRNA-122a and Foxm1 by ISH, IHC and RT-PCR methods, and analyzing the correlation between miRNA-122a and Foxm1. In the cell experiment, Dividing DU-145 and PC-3 as 3 groups: NC groups, BL groups and miRNA groups. Using transwell and wound healing test to evaluate cell invasion and migration abilities. Using WB test to measure the relative proteins levels. Results: miRNA-122a and Foxm1 expressions of tumor tissues was significantly differences compared with adjacent normal tissues (P < 0.05y ). MiRNA-122a was negative correlation with Foxm1 in prostatic cancer tissues. The invasion cell number and wound healing rate of miRNA groups were significantly down-regulation compared with NC groups in DU-145 and PC-3 (P < 0.05). The relative proteins levels of miRNA groups were significantly differences compared with NC in DU-145 and PC-3 (P < 0.05). Conclusion : miRNA-122a might be a suppressor biomarker in the prostatic cancer.
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Chang, Chih-Hui, Hung-Pei Tsai, Shih-Hsun Kuo, Joon-Khim Loh, Chien-Ju Lin, Chih-Lung Lin, and Aij-Lie Kwan. "Synthetic Triterpenoid CDDO-Me Inhibits Proliferation, Migration, and Invasion in GBM8401 and GBM8901." International Surgery 104, no. 3-4 (March 1, 2020): 90–98. http://dx.doi.org/10.9738/intsurg-d-20-00005.1.
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Objectives: We determined the anticancer potency of CDDO-Me in glioblastoma cell lines and the underlying mechanisms in vitro. Summary: CDDO-Me is a synthetic triterpenoid with more potent anticancer and cancer preventive actions compared with the original triterpenoid CDDO. Methods: Two glioblastoma cell lines, GBM8401 and GBM8901, were utilized to test the effect of CDDO-Me on cell viability, cell migration, and cell invasion using the MTT, wound healing, and transwell migration assays, respectively. Additionally, Western blotting was used to determine the protein expression levels of N-cadherin, cyclin D1, and vascular endothelial growth factor. Results: At nanomolar concentrations, CDDO-Me inhibited proliferation, migration, and invasion in both cell lines. In addition, CDDO-Me exhibited a dose-dependent downregulation in the protein levels of N-cadherin, cyclin D1, and vascular endothelial growth factor in GBM8401 and GBM8901 cells. Conclusions: CDDO-Me exhibited anticancer effects at low nanomolar concentrations and should be considered as a potential chemotherapeutic agent for glioblastoma.
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Cai, Hui, and Hongmei Deng. "Long Non-Coding Sprouty4-Intronic Transcript 1 (SPRY4-IT1) Regulates Cancer Biological Effects and Cisplatin Sensitivity in Cervical Cancer." Journal of Biomaterials and Tissue Engineering 9, no. 6 (June 1, 2019): 789–96. http://dx.doi.org/10.1166/jbt.2019.2060.
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Background: Emerging evidences have revealed that Long noncoding RNAs (LncRNAs) is crucial for cancer progression. Previous studies have elucidated that patients with higher LncRNA SPRY4IT1 was more advanced. This study aims to investigate the biological effects of LncRNA SPRY4-IT1 and preliminary explore the effects of LncRNA SPRY4-IT1 on cisplatin sensitivity. Materials and methods: Quantitative reverse transcriptase PCR was used to validate the expression of SPRY4IT1. Cell migration and invasion were detected by scratch test and Transwell assay. Cell cytometry was performed for cell apoptosis. The expression of proteins was evaluated by immunoblotting. The drug sensitivity was measured by CCK-8. Results: LncRNA SPRY4-IT1 was significantly expressed in cervical cancer cell lines compared to normal cells. Downregulation of LncRNA SPRY4-IT1 in cervical cancer cells suppress the cell viability, cell invasion and migration and promoted apoptosis. In addition, decreases of LncRNA SPRY4-IT1 enhanced the cisplatin sensitivity in cervical cell lines. Conclusion: LncRNA SPRY4-IT1 is a potential biomarker and therapy target for cervical cancer.
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Li, Xiao-Na, Hong Yang, and Tao Yang. "miR-122 Inhibits Hepatocarcinoma Cell Progression by Targeting LMNB2." Oncology Research Featuring Preclinical and Clinical Cancer Therapeutics 28, no. 1 (February 7, 2020): 41–49. http://dx.doi.org/10.3727/096504019x15615433287579.
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In the present study, we investigated the role of miR-122 in hepatocarcinoma progression and explored the mechanism. In hepatocarcinoma tissues and cells, we used qRT-PCR to validate the miR-122 expression level. Next, we used colony formation by crystal violet staining assay to compare cell proliferation ability, and we used scratch test or Transwell assay to compare cell migration or invasion ability. We then conducted bioinformatics or luciferase reporter gene assay to prove the regulation effect of miR-122 on lamin B2 (LMNB2), and the biological function of LMNB2 was analyzed. We used nude mouse tumorigenicity assay to test the inhibition effect of miR-122 ASO therapy against hepatocarcinoma. miR-122 was reduced in hepatocarcinoma tissues compared to the paracarcinoma tissues, which was relatively low or high in hepatocarcinoma cell line SMMC7721 or Hep3B, and overexpressed miR-122 inhibited proliferation, migration, and invasion in hepatocarcinoma cells. Additionally, some reports showed that LMNB2 was regulated by miR-122, which inhibited the expression of LMNB2. Moreover, LMNB2 functioned to promote cell proliferation, migration, and invasion. We could achieve the inhibition of hepatocarcinoma using miR-122 therapy through decreasing LMNB2 expression in vivo. Our data indicated that miR-122 could inhibit hepatocellular carcinoma cell progression by targeting LMNB2 and as a therapeutic target for hepatocarcinoma treatment.
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Yu, Bohan, Qin Li, and Fang Wang. "Effects of Transforming Growth Factor-/β 1 and Concentrated Growth Factor on Growth, Proliferation and Osteogenic Differentiation of Bone Marrow Stem Cells." Journal of Biomaterials and Tissue Engineering 11, no. 1 (January 1, 2021): 185–93. http://dx.doi.org/10.1166/jbt.2021.2397.
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Objective: We aimed to explore the effects of transforming growth factor-β1 (TGF-β1) and concentrated growth factor (CGF) on growth, proliferation and osteogenic differentiation of bone marrow stem cells (BMSCs). Methods: CGF was extracted from rat venous blood. BMSCs was isolated from rats. TGF-β1 or CGF was used to induced BMSCs to observe their effects on BMSCs. The expression levels of BMSCs surface antigens were detected by flow cytometry. ELISA was performed to test the expression of VEGF, TGF-β1, PDGF and SDF-1 in BMSCs. qRT-PCR was carried out to test the expression of COL-I, OPN, OC and ALP in BMSCs. Transwell assay was used to detect the migration rates of BMSCs. The cell morphology of BMSCs was detected by Alizarin red staining. Results: BMSCs were successfully isolated from rats. CGF could significantly increase the expression of TGF-β1, PDGF and VEGF in BMSCs. In addition, TGF-β1 and CGF notably increased the proliferation of BMSCs. And they not only improved the activity of ALD, but also increased the levels of ALP, OPN, COL-I and OCN in BMSCs to prompt the growth of BMSCs. Conclusion: CGF combined with TGF-β1 could prompt the growth, proliferation and osteogenic differentiation of BMSCs.
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Mun, Yeung-Chul, Soo Ah Oh, Kyoung-Eun Lee, Eun-Sun Yoo, Hye-Jung Chang, Moon-Young Choi, Jee-Young Ahn, Jae-Hong Kim, and Chu-Myong Seong. "Hematopoietic Stem Cells Mobilization by G-CSF and LTB4 Was Significantly Suppressed by an Oxygen Radical Scavenger or an Inhibitor of NADPH Oxidase." Blood 110, no. 11 (November 16, 2007): 4911. http://dx.doi.org/10.1182/blood.v110.11.4911.4911.
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Abstract Introduction: We previously had reported that LTB4 was able to mobilize HSC within 4 hours without significant side effects and that LTB4 receptor was involved in both of the pathways of mobilization induced by G-CSF and LTB4 in the murine model. Though the roles of protease (ie. NE, MMPs) seem to be important, the precise mechanisms are still unknown. ROS (reactive oxygen species) have cell signaling roles that are involved in signal transduction cascades of numerous growth factor-, cytokine-, and hormone-mediated pathways, and regulate many biological systems. Because a variety of inflammatory cytokines and chemokines, including G-CSF and LTB4, induce a rapid increase of intracellular ROS, we hypothesized that the role of ROS on HSC mobilization induced by G-CSF and LTB4 might be important. Methods: MS5, murine stromal cell line cells, or bEnd3, murine microvascular cell line cells, were grown to confluence on the microporous transwell membrane. Murine marrow cells were placed on top of the prepared transwell membrane. The transwells were then seated in wells containing media and G-CSF or LTB4 with or without pretreatment of NAC, an oxygen free radical scavenger, or DPI, an inhibitor of NADPH oxidase-like flavoproteins. Cells that migrated through the stromal or endothelial layer into the wells were assayed for mobilization. NAC and DPI were given to C57BL/6 mice followed by rhG-CSF (5μg, IV) or LTB4 (1μg, IV) after a period of 2 hours. 24 hours after the rhG-CSF injection or 4 hours after the LTB4 injection, peripheral blood samples were obtained via cardiac puncture. The samples were analyzed for TNC using a trypan blue stain and FACS analysis were performed using Sca-1 and lineage markers, including CD45R (B220), CD116, Gr-1 and TER119. Results: The numbers of migrated cell through the MS5 or bEnd3 were increased by treatment of G-CSF or LTB4. However, increasing effects of G-CSF or LTB4 to the transmigration through the MS5 or bEnd3 were inhibited by pretreatment of NAC or DPI. Comparing the control arm, the numbers of WBC and HSC (Sca-1+Lin−) in blood were decreased in the G-CSF or LTB4 mobilized mice (N=4), in which NAC or DPI were pretreated (Sca-1+Lin− fraction in peripheral blood: 1.91±0.80% in G-CSF alone, 0.55±0.37% in G-CSF with NAC, 0.36±0.09% in G-CSF with DPI, P<0.05; 1.92±0.49% in LTB4 alone, 0.55±0.29% in LTB4 with NAC, 0.67±0.52% in LTB4 with DPI, P<0.05). Conclusions: Through our data, it is suggested that ROS are involved in the HSC mobilization induced by G-CSF and LTB4 in the murine model. It would be very interesting to test the effect of G-CSF or LTB4 on ROS K/O mice in the future. As for now, we will try to find the critical signal transduction pathway, through which we may find more effective and efficient molecules for HSC mobilization.
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Hu, Qingfeng, Shijun Tong, Xiaojun Zhao, Weihong Ding, Yuancheng Gou, Ke Xu, Chuanyu Sun, and Guowei Xia. "Periostin Mediates TGF-β-Induced Epithelial Mesenchymal Transition in Prostate Cancer Cells." Cellular Physiology and Biochemistry 36, no. 2 (2015): 799–809. http://dx.doi.org/10.1159/000430139.
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Background: In our previous study, we found that periostin was upregulated in prostate cancer, and its expression could be modulated by TGF-β. TGF-β could upregulate periostin expression in some cells, and both TGF-β and periostin could induce epithelial mesenchymal transition (EMT). We aimed to study the effect of periostin in the process of TGF-β-induced EMT in prostate cancer cells. Methods: We constructed a lentivirus vector containing the periostin gene and transduced it into PC3 and DU145 cells. After confirming periostin overexpression by PCR and Western blotting, we used an MTT assay to establish a growth curve to measure cell proliferation. Additionally, we performed transwell and wound healing assays to measure cell invasion and migration, respectively. Lastly, we measured the expression of EMT associated factors using Western blot analysis to test the effect of periostin on EMT in prostate cancer cells. Results: PCR and Western blot analyses confirmed that periostin was upregulated after infection with the periostin lentiviral vector. Periostin overexpression promoted increased cell proliferation, invasion, and migration as measured by MTT, transwell, and wound healing assays, respectively. Western blot analysis illustrated that periostin overexpression increased the expression of EMT associated factors, and periostin overexpression activated Akt and GSK-3β, which could be inhibited using a PI3K inhibitor. Additionally, TGF-β increased the levels of STAT3, Twist1 and periostin, while both STAT3 shRNA and Twist1 shRNA inhibited periostin expression. However, STAT3 shRNA also decreased Twist1 expression. Although reduction of STAT3, Twist1 or periostin levels with shRNA inhibited TGF-β-induced overexpression of EMT associated factors, periostin overexpression could reverse such inhibition by interfering with STAT3 and Twist1. Similarly, periostin overexpression also reversed inhibition of cell invasion induced by interference of STAT3 and Twist1. Conclusion: Our findings indicate that periostin is an important mediator of TGF-β-induced EMT and suggest that periostin is a potential therapeutic target for suppressing the metastatic progression of prostate cancer.
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Mao, Yuan, Qi Tang, Weifei Fan, Xiaojun Tang, Li Xu, Jin Zhu, Zhenqing Feng, and Jun Wang. "A novel MAGE-A1-IgG antibody for lung adenocarcinoma." Journal of Clinical Oncology 35, no. 15_suppl (May 20, 2017): e20085-e20085. http://dx.doi.org/10.1200/jco.2017.35.15_suppl.e20085.
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e20085 Background: Melanoma-associated antigen A1 (MAGE-A1) has been reported to perform oncogenically and act as an ideal candidate in tumor immunotherapy. Methods: One-step quantitative real-time polymerase chain reaction (qPCR) test and immunohistochemistry (IHC) analysis were used to detect the relationship between MAGE-A1 expression and the clinicopathological characteristics of lung adenocarcinoma (LAC). Then a novel MAGE-A1 IgG antibody was constructed on the previous MAGE-A1 scFv antibody by eukaryotic expression vectors. CCK-8, wound healing, transwell, matrigel, apoptosis, antibody-dependent cell-mediated cytotoxicity (ADCC) and CDC (complement-dependent cytotoxicity) assays were performed to evaluate the inhibitory effects of MAGE-A1-IgG on LAC in vitro. Results: High MAGE-A1 expression was observed in LAC tissues and MAGE-A1 expression was associated with several malignant properties of LAC patients, including overall survival. MAGE-A1-IgG revealed significant roles in inhibiting proliferation, inducing apoptosis and activating ADCC and CDC of LAC in a dose- and time- dependent manner in vitro. Conclusions: MAGE-A1-IgG may provide a promising therapeutic strategy for the treatment of MAGE-A1-positive LAC.
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Yu, Zhijuan, Liguo Wang, and Xiujuan Li. "MiR-3150b-3p inhibits the proliferation and invasion of cervical cancer cells by targeting TNFRSF11a." Journal of Investigative Medicine 68, no. 6 (July 2, 2020): 1166–70. http://dx.doi.org/10.1136/jim-2020-001284.
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The objective of this study was to determine the role of miR-3150b-3p in the cervical cancer (CC) progression. Real-time PCR and western blot analysis were conducted to test the expression of miR-3150b-3p, TNFRSF11a and p38 mitogen-activated protein kinase (MAPK) signaling pathway. The interaction between miR-3150b-3p and TNFRSF11a was verified by luciferase assay. Cell proliferation, migration and invasion were determined by CCK-8, wound healing and Transwell assays. In this study, we showed that miR-3150b-3p was significantly downregulated in CC cell lines. Additionally, miR-3150b-3p markedly attenuated the proliferation, migration and invasion of HeLa and SiHa cells. Moreover, we identified TNFRSF11a to be a novel target of miR-3150b-3p in CC cells. Enforced expression of TNFRSF11a abolished the antitumor effect of miR-3150b-3p. Besides, miR-3150b-3p was involved in the regulation of the p38 MAPK signaling pathway. In conclusion, our data suggested that miR-3150b-3p directly targets TNFRSF11a to inactivate the p38 MAPK signaling pathway, thus implicating miR-3150b-3p in the regulation of CC cell growth.
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Luo, Baochang, and Jing Zhang. "MicroRNA-16 inhibits the migration and invasion of glioma cell by targeting Bcl-2 gene." Tropical Journal of Pharmaceutical Research 19, no. 12 (March 12, 2021): 2499–504. http://dx.doi.org/10.4314/tjpr.v19i12.3.
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Purpose: To investigate the effect of microRNA-16 (miR-16) on glioma cell migration and invasiveness, and the mechanism involved.Methods: MicroRNA-16 mimic or inhibitor was transfected into human glioma (SHG44) cells. Cell migration, invasiveness and morphology were determined using scratch test, Transwell invasion assay, and immunohistochemical staining, respectively. Expressions of bcl-2, MMP-9 and MMP-2, and NF-κB1 proteins were measured using Western blotting.Results: Overexpression of MicroRNA-16 significantly down-regulated MMP-9 protein in SHG44 cells (p < 0.05), but MMP-2 protein expressions in the 2 groups were comparable (p > 0.05). Protein expressions of MMP-9 and NF-κB1 were significantly down-regulated in human glioma positive cells, relative to negative control.Conclusion: MiR-16 overexpression suppresses the migration and invasiveness of SHG44 cells via the regulation of NF-κB1/MMP-9 signaling pathway, and it directly targets bcl-2 gene by inhibiting its protein expression. This finding affords a new target for developing new anti-glioma drugs.
Keywords: Bcl-2, Expression, Glioma, MicroRNA-16, NF-κB1signaling pathway
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Yang, Yang, Fangyuan Yin, Qiyun Hang, Xiaoliang Dong, Jiao Chen, Ling Li, Peng Cao, Zhimin Yin, and Lan Luo. "Regulation of Endothelial Permeability by Glutathione S-Transferase Pi Against Actin Polymerization." Cellular Physiology and Biochemistry 45, no. 1 (2018): 406–18. http://dx.doi.org/10.1159/000486918.
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Background/Aims: Inflammation-induced injury of the endothelial barrier occurs in several pathological conditions, including atherosclerosis, ischemia, and sepsis. Endothelial cytoskeleton rearrangement is an important pathological mechanism by which inflammatory stimulation triggers an increase of vascular endothelial permeability. However, the mechanism maintaining endothelial cell barrier function against inflammatory stress is not fully understood. Glutathione S-transferase pi (GSTpi) exists in various types of cells and protects them against different stresses. In our previous study, GSTpi was found to act as a negative regulator of inflammatory responses. Methods: We used a Transwell permeability assay to test the influence of GSTpi and its transferase activity on the increase of endothelial permeability induced by tumor necrosis factor alpha (TNF-α). TNF-α-induced actin remodeling and the influence of GSTpi were observed by using laser confocal microscopy. Western blotting was used to test the influence of GSTpi on TNF-α-activated p38 mitogen-activated protein kinase (MAPK)/MK2/heat shock protein 27 (HSP27). Results: GSTpi reduced TNF-α-induced stress fiber formation and endothelial permeability increase by restraining actin cytoskeleton rearrangement, and this reduction was unrelated to its transferase activity. We found that GSTpi inhibited p38MAPK phosphorylation by directly binding p38 and influenced downstream substrate HSP27-induced actin remodeling. Conclusion: GSTpi inhibited TNF-α-induced actin remodeling, stress fiber formation and endothelial permeability increase by inhibiting the p38MAPK/HSP27 signaling pathway.
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Wen, Ting, Boyi Niu, Qiaoli Wu, Yixian Zhou, Xin Pan, Guilan Quan, and Chuanbin Wu. "Fenofibrate Solid Dispersion Processed by Hot-Melt Extrusion: Elevated Bioavailability and Its Cell Transport Mechanism." Current Drug Delivery 16, no. 6 (August 27, 2019): 538–47. http://dx.doi.org/10.2174/1567201816666190122123044.
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Background: Fenofibrate (FNB) is an effective drug for the treatment of hypertriglyceridemia, hypercholesterolemia as well as mixed hyperlipidemia. However, due to its poor aqueous solubility, FNB has the problem of poor oral absorption followed by low bioavailability. Objective: The aim of this research was to construct FNB amorphous solid dispersion employing PVP VA64 as the carrier by hot-melt extrusion method, in order to improve the oral bioavailability. Additionally, the cell transport experiment was conducted to further investigate the mechanism of promoted osmotic absorption. Methods: The physical state of the obtained solid dispersion was characterized using SEM, DSC and XRD. Besides, in vitro Caco-2 cells were used to evaluate the cytotoxicity of the carrier and mimic gastrointestinal drug permeation. At last, in vitro dissolution test and in vivo bioavailability study were also carried out. Results: The prepared FNB solid dispersion was found to be an amorphous state after hot-melt extrusion process. In vitro cytotoxicity test on Caco-2 cells confirmed the excellent biocompatibility of the carrier PVP VA64. Besides, transwell cell transport assay and in vitro dissolution test revealed that FNB released from amorphous solid dispersion was equipped with an improved transmembrane transport and dissolution rate. Moreover, pharmacokinetic study in beagle dogs showed that comparing with commercial micronized product Lipanthyl®, the oral bioavailability of FNB solid dispersion was significantly enhanced (2.45 fold). Conclusion: In conclusion, PVP VA64 can be regarded as a promising polymer to enhance the bioavailability of poorly water-soluble drugs such as FNB processed by hot-melt extrusion. Besides, investigations on the mechanism of the enhanced penetration are expected to lay a foundation on the subsequent development of effective and practical solid dispersion.
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Chen, Sangsang, Xuqing Zhu, Jing Zheng, Tingting Xu, Yinmin Xu, and Feng Chen. "miR-30a-5p Regulates Viability, Migration, and Invasion of Lung Adenocarcinoma Cells via Targeting ECT2." Computational and Mathematical Methods in Medicine 2021 (July 7, 2021): 1–12. http://dx.doi.org/10.1155/2021/6241469.
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Objective. The abnormal expression of epithelial cell transforming sequence 2 (ECT2) is often considered the driving factor for the growth and invasion of tumors. This study was performed to investigate the regulatory effect of miR-30a-5p and ECT2 on lung adenocarcinoma (LUAD), which provides a basis for the effective clinical treatment of LUAD. Methods. The mature miRNAs, expression data of mRNAs, and clinical data of LUAD were downloaded from The Cancer Genome Atlas (TCGA). The expression levels of ECT2 mRNA and miR-30a-5p in cancer cell lines were detected by qRT-PCR. Western blot was performed to test the expression of ECT2 protein. The targeting relationship between miR-30a-5p and ECT2 was verified by dual-luciferase assay. The CCK-8 method and Transwell assay were conducted to test the viability, migratory, and invasive abilities of cells. Results. ECT2 expression was upregulated in LUAD and was significantly correlated with the LUAD clinical stage and pathologic T stage, and the expression of its upstream regulatory gene miR-30a-5p was downregulated. miR-30a-5p targeted ECT2 in LUAD. Downregulation of ECT2 could inhibit the viability, migration, and invasion of LUAD cells, which could be reversed by simultaneously suppressing the expression of miR-30a-5p. Conclusion. Our results suggested that miR-30a-5p repressed the malignant progression of LUAD via downregulating ECT2. miR-30a-5p and ECT2 may be effective targets for LUAD patients.
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Hu, Tian, Yongde Xu, Bin Yao, Xiaobing Fu, and Sha Huang. "Developing a Novel and Convenient Model for Investigating Sweat Gland Morphogenesis from Epidermal Stem Cells." Stem Cells International 2019 (February 4, 2019): 1–7. http://dx.doi.org/10.1155/2019/4254759.
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Sweat glands developed from the embryonic epidermis. To elucidate the underlying mechanisms of morphogenesis, a reliable in vitro test system for bioactive screening must be developed. Here, we described a novel and convenient model by coculturing embryonic tissue and epidermal stem cells (ESCs) using Transwell insert for evaluating the effects of soluble morphogens on sweat gland morphogenesis in vitro. Using this coculture system, morphological alteration, histological features, and specific markers were observed. Initial experiments revealed that ESCs cocultured with embryonic paw pad (EPP) tissue demonstrated glandular structure and cytokeratin 8 (K8) and cytokeratin 18 (K18) positive, while ESCs cocultured with embryonic dorsal skin demonstrated “sea snail” structure and K8, K18 negative. Moreover, bone morphogenetic protein 4 (BMP4) and epidermal growth factor (EGF) concentrations were detected in the medium of the EPP group. BMP receptor inhibitor could effectively block the ESC differentiation to sweat glands, while EGF receptor blocker did not show the effect. Our results showed clear benefits of this novel and convenient model in terms of in vitro-in vivo correlation. It was an appropriate alternative for screening of potential bioactives regulating the sweat gland morphogenesis mechanism.
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Xue, Sheng-Neng, Juan Lei, Chuan Yang, Diao-Zhu Lin, and Li Yan. "The Biological Behaviors of Rat Dermal Fibroblasts Can Be Inhibited by High Levels of MMP9." Experimental Diabetes Research 2012 (2012): 1–7. http://dx.doi.org/10.1155/2012/494579.
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Aims. To explore the effects of the high expression of MMP9 on biological behaviors of fibroblasts.Methods. High glucose and hyperhomocysteine were used to induce MMP9 expression in skin fibroblasts. Cell proliferation was detected by flow cytometry and cell viability by CCK-8. ELISA assay was used to detect collagen (hydroxyproline) secretion. Scratch test was employed to evaluate horizontal migration of cells and transwell method to evaluate vertical migration of cells.Results. The mRNA and protein expressions of MMP9 and its protease activity were significantly higher in cells treated with high glucose and hyperhomocysteine than those in control group. At the same time, the S-phase cell ratio, proliferation index, cell viability, collagen (hydroxyproline) secretion, horizontal migration rate, and the number of vertical migration cells decreased in high-glucose and hyperhomocysteine-treated group. Tissue inhibitor of metalloproteinase 1 (TIMP1), which inhibits the activity of MMP9, recovered the above biological behaviors.Conclusions. High expression of MMP9 in skin fibroblasts could be induced by cultureing in high glucose and hyperhomocysteine medium, which inhibited cell biological behaviors. Inhibitions could be reversed by TIMP1. The findings suggested that MMP9 deters the healing of diabetic foot ulcers by inhibiting the biological behaviors of fibroblasts.
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Zhang, Yuan-yuan, Ying-mei Zhang, and Hai-yan Xu. "Effect of Codonopsis pilosula Polysaccharides on the Growth and Motility of Hepatocellular Carcinoma HepG2 Cells by Regulating β-Catenin/TCF4 Pathway." International Journal of Polymer Science 2019 (May 8, 2019): 1–7. http://dx.doi.org/10.1155/2019/7068437.
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Objective. To study the effect of Codonopsis pilosula polysaccharide (CPP) on the growth and motility of HepG2 cells and its possible mechanism. Methods. Cells were randomly divided into Control group, CPP (5 μM) group, CPP (10 μM) group, and CPP (20 μM) group. The proliferation, invasion, migration ability, and expression of proteins involved in the epithelial-mesenchymal transition (EMT) and signaling pathway of HepG2 cells were detected by CCK8 assay, BrdU staining, Transwell, Scratch test, and Western blot, respectively. Results. Codonopsis pilosula polysaccharide inhibited the proliferation of HepG2 cells cultured in vitro along with the expression level of Ki67 and PCNA protein (P<0.05), decreased the number of invasive cells (P<0.05), and reduced the scratch closure rate (P<0.05). It also adjusted the expression of vascular endothelial growth factor (VEGF), E-cadherin, and N-cadherin (P<0.05). Other than that, downregulation of β-catenin, TCF4, and c-Myc protein expression (P<0.05) was observed as well. Conclusion. Codonopsis pilosula polysaccharide can inhibit the proliferation and motility of HepG2 cells cultured in vitro, and the underlying mechanism is proposed to be related to the inhibition of the β-catenin/TCF4 pathway.
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Liu, Yongze, Han Zhou, Xiaofeng Ma, Chuanyao Lin, Ling Lu, Dingding Liu, Dengbin Ma, Xia Gao, and Xiao Yun Qian. "Prodigiosin Inhibits Proliferation, Migration, and Invasion of Nasopharyngeal Cancer Cells." Cellular Physiology and Biochemistry 48, no. 4 (2018): 1556–62. http://dx.doi.org/10.1159/000492278.
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Background/Aims: Nasopharyngeal carcinoma remains a devastating and difficult disease to treat. This study explores the antineoplastic effect of prodigiosin on nasopharyngeal cancer cells. Methods: Human nasopharyngeal carcinoma CNE2 cells and human normal nasopharyngeal epithelial NP69 cells were obtained and treated with prodigiosin or fluorouracil (5-FU). Colony formation assay was performed to screen for the optimal experimental concentrations of prodigiosin and 5-FU, and MTT assay was used to examine cell proliferative ability. Flow cytometry was used to examine cell cycle distribution, the scratch test was employed to examine cell migration, and Transwell migration assay (Boyden chamber) was used to study cell invasion. Results: The optimal concentrations of prodigiosin and 5-FU for treatment were 4 mg/L and 0.35 mg/L, respectively. Both prodigiosin and 5-FU inhibited tumor cell proliferation. The percentage of cells in G0/G1 phase was higher and the percentage of cells in S phase was lower in the prodigiosin and 5-FU groups than in the untreated groups. Both prodigiosin and 5-FU inhibited tumor cell migration and tumor cell invasion. Conclusions: Our results suggest that prodigiosin can inhibit proliferation, migration, and invasion of nasopharyngeal carcinoma cells.
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He, Zhicheng, Yang Xia, Chunfeng Pan, Teng Ma, Bin Liu, Juejin Wang, Liang Chen, and Yijiang Chen. "Up-Regulation of MiR-452 Inhibits Metastasis of Non-Small Cell Lung Cancer by Regulating BMI1." Cellular Physiology and Biochemistry 37, no. 1 (2015): 387–98. http://dx.doi.org/10.1159/000430362.
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Background/Aims: MicroRNAs (miRNAs) have been regarded as a new class of regulators in cellular processes in non-small cell lung cancer (NSCLC). However, the relationship between miR-452 and the development of NSCLC remains unclear. Methods: qRT-PCR was used to detect the expression of miR-452 and its target gene in NSCLC samples (n=60). The transwell assay was used to test the cell invasion capability. The regulation mechanism was confirmed by luciferase reporter assay and western blot assay. Results: In the current study, a relatively lower miR-452 and higher BMI1 expression levels were confirmed to be associated with advanced tumor stage and more extent of lymph nodes metastasis. In vitro, down-regulated miR-452 could enhance cell invasion capability. Furthermore, miR-452 modulated BMI1 expression by binding to its 3ʹ-UTR. The enhancement of cell invasion capability induced by down-regulated miR-452 was eliminated by repression of BMI1. Conclusions: Our results suggest that miR-452 plays a vital role in development of NSCLC, and this miR-452-BMI1 pathway might generate a novel insight into the treatment of NSCLC.
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Poggio, Claudio, Matteo Ceci, Alberto Dagna, Riccardo Beltrami, Marco Colombo, and Marco Chiesa. "In vitro cytotoxicity evaluation of different pulp capping materials: a comparative study." Archives of Industrial Hygiene and Toxicology 66, no. 3 (September 1, 2015): 181–88. http://dx.doi.org/10.1515/aiht-2015-66-2589.
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Abstract Direct pulp capping covers the exposed surface of the pulp to maintain its vitality and preserve its functional and biologic activity. The aim of the present study was to compare the biocompatibility effects of seven different pulp-capping materials in vitro: Dycal®, Calcicur®, Calcimol LC®, TheraCal LC®, ProRoot MTA®, MTA-Angelus®, and Biodentine®. Using the Transwell insert methodology by Alamar blue test, we evaluated the cytocompatibility of the above mentioned materials towards murine odontoblasts cells (MDPC-23) at three different times (24, 48, and 72 h). For additional control, the cell viability at 72 hours was also assessed by MTT assay. Morphological analysis of murine odontoblasts was assessed by Confocal Laser Scanning Microscope. The results indicate significantly different biocompatibility among materials with different composition. Biodentine® and mineral trioxide aggregate (MTA)-based products showed lower cytotoxicity, varying from calcium hydroxide-based materials, which exhibited higher cytotoxicity. Although our findings are limited to in vitro conditions, the observation that Biodentine® caused a cytotoxic effect similar to MTA suggests that it may be considered an alternative in pulp-capping treatment, as calcium hydroxide-based materials present higher cytotoxic effects.
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Cai, Hairui, Dongmei Li, Jun Wu, and Chunbo Shi. "miR-519d downregulates LEP expression to inhibit preeclampsia development." Open Medicine 16, no. 1 (January 1, 2021): 1215–27. http://dx.doi.org/10.1515/med-2021-0244.
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Abstract The purpose of the current study was to characterize role of microRNA (miR)-519d in trophoblast cells and preeclampsia (PE) development and its potential underlying mechanism. Regulation of leptin (LEP) by miR-519d was verified using a dual-luciferase reporter gene assay. Loss- and gain-of-function assays were conducted to detect the roles of miR-519d and LEP in proliferation, migratory ability, and invasive capacity of HTR-8/SVneo cells by means of CCK-8 assay, scratch test, and Transwell invasion assay, respectively. The cell apoptosis rate and cycle distribution were analyzed by flow cytometry. LEP expression was elevated, whereas miR-519d level was suppressed in the PE placenta samples compared with those from normal pregnancy. Depletion of LEP promoted proliferation, migratory ability, and invasive capacity and repressed apoptosis. miR-519d could bind 3′ untranslated regions (3′UTRs) of LEP, the extent of which correlated negatively with LEP expression. miR-519d suppressed the expression of LEP in HTR-8/SVneo cells. Moreover, overexpression of miR-519d promoted survival and migratory ability of HTR-8/SVneo cells. Taken together, we find that miR-519d targeted LEP and downregulated its expression, which could likely inhibit the development of PE.
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Tao, Xiao-Ling, Wei-Chang Yu, De-Jun Chen, Li-Ming Wang, Lu Liu, and Qi Xing. "Hepatocyte Nuclear Factor -1α stimulates cervical cancer cells to migrate and invade through regulating pyruvate kinase L/R." Investigación Clínica 62, no. 3 (September 2, 2021): 236–46. http://dx.doi.org/10.22209/ic.v62n3a05.
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This study was aimed to analyze the role of hepatocyte nuclear factor -1α (HNF-1α) in regulating migrative and invasive potentials in cervical cancer via the involvement of pyruvate kinase L/R (PKLR). The expression of HNF-1α and PKLR in cervical cancer tissues classified by tumor size and FIGO (Federation International of Gynecology and Obstetrics) stage were detected by qRT-PCR. The expression correlation between HNF-1α and PKLR in cervical cancer tissues was analyzed by Pearson correlation test. After intervening HNF-1α and PKLR levels in SiHa and Hela cells, their migratory and invasive abilities were examined by the Transwell assay. HNF-1α was upregulated in cervical cancer tissues, particularly those with large tumor size or advanced FIGO stage. PKLR was highly expressed in cervical cancer tissues as well, presenting a positive correlation with the HNF-1α level. Knockdown of HNF-1α attenuated migratory and invasive abilities in SiHa cells, whereas overexpression of HNF-1α enhanced migratory and invasive abilities in SiHa cells. PKLR was able to abolish the regulatory effects of HNF-1α on cervical cancer metastasis. HNF-1α and PKLR synergistically promote cervical cancer to migrate and invade.
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Song, Xin, Shuai Zhang, Shouchuan Li, Ye Wang, Xinming Zhang, and Feng Xue. "Expression of the CLCA4 Gene in Esophageal Carcinoma and Its Impact on the Biologic Function of Esophageal Carcinoma Cells." Journal of Oncology 2021 (June 4, 2021): 1–7. http://dx.doi.org/10.1155/2021/1649344.
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Background. Esophageal carcinoma (ESCA) is one of the malignant tumors with a high mortality rate worldwide, which seriously affects people’s health. Calcium-activated chloride channel 4 (CLCA4) was reported to be a tumor inhibitor in hepatocellular carcinoma. Nevertheless, the role of CLCA4 in ESCA is still unclear. Methods. RT-qPCR and western blot assay were used to test the expression pattern of CLCA4 in ESCA tissues and cells. CCK-8 assay was performed to detect the effect of CLCA4 overexpression on cell proliferation in ESCA cells. Transwell assay was used to measure the effect of CLCA4 upregulation on migration and invasion abilities of ESCA cells. Animal experiments were conducted to investigate the role of CLCA4 upregulation in tumor growth in vivo. Results. CLCA4 was significantly reduced in ESCA tissues and correlated with T stage, differentiation, and lymph node metastasis. CLCA4 overexpression was found to inhibit cell proliferation, migration, invasion, and EMT progression in ESCA cells. Moreover, CLCA4 overexpression suppressed tumor growth in vivo. Conclusion. CLCA4 was suggested to act as a tumor inhibitor in ESCA and might be a therapeutic target gene for the treatment of patients with ESCA.
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Melo, Rita de Cassia Carvalho, Juliana M. Xavier-Ferrucio, Lauremilia Ricon, Karla Priscila Vieira Vieira Ferro, Carolina L. Bigarella, Gilberto C. Franchi, Alexandre Nowill, and Sara Teresinha Olalla Saad. "CXCR7 Participates in Chemotaxis and Homing Mediated By CXCL12." Blood 126, no. 23 (December 3, 2015): 3601. http://dx.doi.org/10.1182/blood.v126.23.3601.3601.
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Abstract Hematopoiesis is tightly orchestrated by a precise quiescence/cycling equilibrium that is required for the continuous controlled production of differentiated blood cells. Chemokines and their receptors play an essential role in maintaining the hematopoietic cells pool within cell niches. The CXCL12/CXCR4 axis has been identified as the central axis for migration, adhesion and homing of hematopoietic cells and for leukemic cells. Another CXCL12-binding receptor has recently, been identified, CXCR7, however the contribution of this receptor to CXCL12 - mediated effects in hematopoietic cells, is still controversial, even though the CXCR7 relationship with tumor progression in non-hematopoietic malignancies is well established. We recently demonstrated that CXCR7 is highly expressed in acute lymphoid leukemic (ALL) cells and that CXCR7 contributed to T-ALL cell chemotaxis induced by CXCL12 potentializing CXCR4 response. The mouse model with reduced expression of Arhgap21+/- exhibits a 71% downregulation of CXCR7 protein in membrane of T cells, probably due to lower recruitment by β-arrestin since GPCRs recycling to the membrane needs association with this protein. Moreover, this model showed reduction in chemotaxis, adhesion and homing of hematopoietic stem and progenitor cells suggesting that Arhgap21 may be a strong candidate for CXCL12/CXCR4 axis regulation. Thus, in the present study we aimed to investigate the involvement of CXCR7 in chemotaxis induced by CXCL12 and homing using U937 myeloid leukemic cell line in NOD/SCID mice and T-lymphocytes in Arhgap21+/- mice. The subcellular location of CXCR4 and CXCR7 by confocal microscopy evidenced both receptors in the membrane and cytoplasm of U937 cells. After CXCL12 induction, the blocked of CXCR4 by AMD3100 and/or the inhibition of CXCR7 by transduction with lentivirus mediated shRNA resulted in significant changes in U937 cells chemotactic response analyzed by transwell assay (U937 treated with AMD3100, p=0.0019; U937 shCXCR7, p<0.001;U937 shCXCR7 treated with AMD3100, p=0.0056; Mann-Whitney test) and homing assay to spleen of NOD/SCID mouse after 16 hours of transplant (U937 treated with AMD3100, p=0.0070; U937 shCXCR7, p=0.044 6; U937 shCXCR7 treated with AMD3100, p=0.0243, Student's t test). Bone marrow analysis of Arhgap21+/- mice showed a reduction of T lymphocytes (CD4+ andCD8+; p=0.02, Student's t test), erythroblasts (Ter119+, p=0.01) and myeloid cells (Gr1+ Mac+, p=0.02), but there was no difference however in B lymphocytes (B220+). Indeed, peripheral blood showed a significant reduction in CD8+ cells (p=0.04) but similar amounts of CD4+ cells. Thymus did not show difference in CD4+ and CD8+ populations. Herein, we show by transwell assay a lower response of T lymphocytes to CXCL12 (p=0.0050, Mann-Whitney test), corroborating to the reduced CXCR7 expression observed. No difference in CXCR4 expression was observed in any of the cell types. Taken together, our results suggest that CXCR7 is involved in chemotaxis and homing of T-lymphocytes and myeloid leukemic cells, potentalizing the CXCR4 response. The reduction of T-lymphocytes in bone marrow of Arhgap21+/- mice, may be related to a reduced homing due to the reduction of CXCR7 in the membrane of these cells, which leads to a lower attraction induced by CXCL12 ligant to bone marrow. Moreover, an inhibition of both receptors in myeloid leukemic cells could have a better effect in reducing their homing than the blocking of a single receptor. Disclosures No relevant conflicts of interest to declare.
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Di Marco, Amerigo Mirco, Francesco Autore, Paola Lanuti, Idanna Innocenti, Giuseppe Leone, Alice Ramassone, Angelo Veronese, Renato Mariani Costantini, Luca Laurenti, and Rosa Visone. "Impact of BCR Stimulation on Mir-181b in Chronic Lymphocityc Leukemia." Blood 128, no. 22 (December 2, 2016): 2026. http://dx.doi.org/10.1182/blood.v128.22.2026.2026.
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Abstract B cell receptor (BCR) signaling plays an important pathogenic role in chronic lymphocytic leukemia (CLL) enhancing homing and homeostasis of B-CLL cells and favoring the interaction with the pro-survival stromal lymph node microenvironment. Surface expression of CD69 is required to block the cells in lymphoid compartment while Sfingosine-1-phosphate receptor-1 (S1PR1) is necessary for egress of cells to blood. BCR signaling inhibitors such as Ibrutinib and Acalabrutinib, (anti-bruton tyrosine kinase) or Idelalisib (anti-Phosphatidylinositol 3-kinases ) represent a significant therapeutic advance in CLL. At least some of these drugs are distinctive to lead to an initial lymphocitosis due to rapid release of cells from lymphoid organs to blood, where they die. Changes in microRNAs expression characterize clinical progression of CLL with a strong decrease of miR-181b associated with the more aggressive phase of the disease. In this study we demonstrate that miR-181b is part of the BCR pathway in that it influences the anatomical redistribution of CLL cells from lymph nodes into the blood by balancing the expression of CD69 and S1PR1. We co-cultured MEC_01 and pure B-CLL cells in medium supplemented or not with IgM F(ab')2, specific antibodies for BCR. We observed a significant decrease of miR-181b after 24 hrs of BCR stimulation compared with the same cells cultured in medium without IgM F(ab')2. To establish that this effect was due to the stimulation of the BCR, studies were performed on MEC_01 and in pure B-CLL cells treated separately with 1μM Ibrutinib or 1 μM Idelalisib, which are a potent BCR signaling inhibitors. After 1 hours of treatment the relative expression of miR-181b was assessed noting an increase of the transcription of miR, suggesting that the activation of BCR down regulate the expression of miR-181b. To confirm what we observed in vitro, RNA was isolated from B cells of the CLL patients at different time-point before and after treatment with a BTK inhibitor, Acalabrutinib (ACP-196). We observed a marked increase of miR-181b in the patients in therapy with this drugs compared with respective baseline. Since BTK inhibitors lead to the immediate release of CLL cells from lymphoid tissues to circulation, we evaluated whether this miRNA could be involved in this process. To test this hypothesis MEC01 cells were infected with either LV-miR-181b_coGFP or the LV-CTRL_coGFP after which migration was assessed in transwell assays. The Cells (5 × 105 cells/well) were seeded on top of the transwells and allowed to migrate for 4 h. S1P (100 nM) was added to the lower chamber as a chemo attractant. Transwell assay was performed to determine the migratory capacity of MEC-01 GFP+ cells, mimicking spleen (S1P-) vs blood (S1P+) compartments. Our data indicate that enhanced expression of miR-181b accelerate the migration of B-CLL cells. On the same cells we also evaluated the expression of S1PR1 and CD69. We observed that the restoration of miR-181b down regulated CD69 expression and increased the S1PR1. We also demonstrated that both proteins are direct targets and that the regulation on SIPR1 by the miR-181b occurs through a not canonical way. In conclusion, our findings indicate miR-181b is down regulated by BCR stimulation in CLL cells and that its enhanced expression reduced CD69 while increased S1PR1 by direct targeting. This could facilitate the egress from lymphoid tissue to blood and in turn their death. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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Chiu, Yahui Grace, Jacquelyn Lillis, Rakesh Singh, Jane L. Liesveld, Laura M. Calvi, John M. Ashton, and Omar S. Aljitawi. "Role of RasGRP3 in EPO/EPOR Signaling and Transmigration of Human Hematopoietic CD34+ Cells." Blood 132, Supplement 1 (November 29, 2018): 4531. http://dx.doi.org/10.1182/blood-2018-99-116807.
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Abstract Introduction: Umbilical cord blood (UCB) is a salient source of primitive hematopoietic stem progenitor cells (HSPCs) for bone marrow (BM) reconstitution in patients with hematologic and non-hematologic malignancies. However, a relatively low number of HSPCs in UCB units and poor BM homing efficiency greatly hinders the clinical application of UCB CD34+ cells for transplantation. To overcome these hurdles, we developed two independent strategies that increase CD34+ cell numbers and improve BM homing efficiency of UCB HSPCs. First, we expanded UCB HSPCs by culturing them in decellularized Wharton's jelly matrix (DWJM), a biometric scaffold mimicking the 3-dimenstional (3D) microenvironment of BM. Second, we enhanced the in vitro transmigration and in vivo BM homing efficiency of UCB CD34+ cells by blocking EPO/EPOR signaling. Both approaches enhance UCB CD34+ cell migration toward stromal cell-derived factor 1 (SDF1). In this study, we employed RNA-Seq and RT-PCR approaches to analyze UCB HSPCs treated with EPO and co-cultured with DWJM, aiming to identify molecules that regulate UCB HSPC transmigration via EPO/EPOR signaling. Methods: CD34+ cells from highly enriched UCB units (>90% purity) were treated with EPO for 24 hours and separately co-cultured with DWJM for 1 week. UCB CD34+ cells were collected and subjected to RNA-Seq and real-time PCR (RT-PCR) analyses. In vitro transmigration toward SDF-1 was assessed by transwell assay. To assess the involvement of RasGRP3 in UCB CD34+ cell mobility, cells were treated with 100 nM ingenol-3-angelate (I3A), a diacylglycerol (DAG) analog that specifically targets RAS Guanyl Releasing-Protein 3 (RasGRP3), for 16 hours followed by transwell assay. Anti-EPOR antibody-treated or EPO-treated cells were used as controls. In addition, RasGRP3 gene expression was examined in CD34+ cells from peripheral blood (PB) and BM samples collected from the same donor, and compared to RasGRP3 expression in UCB CD34+ cells. Unpaired, 2-tailed t-test was used to analyze results. Results: RasGRP3 was identified by RNA-Seq from the two independent approaches, EPO treatment and DWJM co-culture. EPO downregulated and DWJM upregulated RasGRP3 gene expression in UCB CD34+ cells. RasGRP3 expression was confirmed by qPCR. UCB CD34+ cells that migrated to the bottom chamber of the transwell assays, a population that has a higher mobility, showed an elevated RasGRP3 gene expression and a decreased EPOR cell surface expression. Activation of RasGRP3 by DAG analog I3A induced a significant increase in RasGRP3 gene expression (control: I3A treatment = 1: 202 ± 58, p=0.00012) that was associated with an enhanced transmigration capability (control: I3A = 41%+/-5: 54%+/- 3, p=0.032). Knocking-down of RasGRP3 in K562 cells, a known EPOR expressing cell line, impaired the transmigration capability of K562. CD34+ cells in peripheral blood (PB) showed a higher level of RasGRP3 gene expression compared to CD34+ cells in BM samples from the same healthy donors. RasGRP3 expression in PB CD34+ cells was significantly higher than BM and UCB CD34+ cells (qPCR signals relative to BM, BM: PB: UCB = 1: 431±65: 21±8, p=0.0012, 0.0023, and <0.0001 for BM vs. PB, BM vs. UCB and PB vs. UCB, respectively). Conclusions: By employing transwell assays, flow cytometry and molecular analyses, we demonstrate for the first time that RasGRP3, a protein responsible for GDP/GTP exchange of Ras, regulates the transmigration ability of human CD34+ cells. In addition, our findings connect RasGRP3 expression to the EPOR-mediated signaling pathway in CD34+ cells. A significantly higher level of RasGRP3 expression in PB CD34+ cells than its counterparts in BM might provide an explanation for why PB HSPCs show relatively faster BM engraftment than BM HSPCs during transplantation. Ongoing follow-up studies will elucidate the molecular mechanism(s) underlying EPOR signaling, which holds clinical potential to improve the BM homing deficiency of UCB CD34+ cells via modulating EPOR and RasGRP3 expression (Figure 1). Disclosures Liesveld: Onconova: Other: DSMB; Abbvie: Honoraria. Aljitawi:Medpace: Consultancy; The University of Rochester Medical Center: Patents & Royalties: Pending patent related to decellularized Wharton's jelly matrix.
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Huck, Claudia, Hernane da Silva Barud, Fernanda Gonçalves Basso, Carlos Alberto de Souza Costa, Josimeri Hebling, and Lucas da Fonseca Roberti Garcia. "Cytotoxicity of New Calcium Aluminate Cement (EndoBinder) Containing Different Radiopacifiers." Brazilian Dental Journal 28, no. 1 (February 2017): 57–64. http://dx.doi.org/10.1590/0103-6440201701023.
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Abstract This study aimed to evaluate the cytotoxicity of a calcium aluminate cement (EndoBinder) containing different radiopacifiers, Bi2O3, ZnO or ZrO2, compared with Mineral Trioxide Aggregate (MTA). According to ISO 10993-12:2012 (E) recommendations, 0.2 g of each cement were applied in transwell inserts and placed in 24-well culture plates containing 1 mL of culture medium (DMEM). After 24 h of incubation, the extracts (DMEM containing components released from the cements) were applied to immortalized odontoblast-like MDPC-23 cells. Cell viability (MTT test), alkaline phosphatase activity (ALP), total protein production and cell morphology (Scanning Electron Microscopy - SEM) were evaluated. The volume of 50 µL of extract was used to determine the chemical elements released by the cements using Energy Dispersive Spectroscopy (EDS). The following groups were established (n=6): NC - negative control (without treatment); EB - EndoBinder without radiopacifier; EBBO - EndoBinder+Bi2O3; EBZnO - EndoBinder+ZnO; EBZrO - EndoBinder+ZrO2 and WMTA - White MTA. Data were subjected to statistical analysis (Kruskal-Wallis test, level of significance=5%). Cells exposed to the different versions of EndoBinder presented small reduction in viability, total protein production and ALP activity, with values similar to the NC and WMTA groups (p>0.05). Different elements (C, O, Na, Al, P, Si, Cl, Bi, K) released by the cements were detected in the extracts. However, the cells had no significant changes in their morphology. EndoBinder and MTA did not affect negatively the metabolism of the odontoblastic-like cells, showing it to be cytocompatible, irrespective of the used radiopacifier.
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Liu, Xiao, Yuanlan Chen, and Zhijiao Jiang. "Grifolin Inhibits Proliferation, Migration, and Invasion of Lung Cancer A549 Cells by Regulating miRNA-1251-5p." Nanoscience and Nanotechnology Letters 12, no. 3 (March 1, 2020): 376–82. http://dx.doi.org/10.1166/nnl.2020.3114.
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To investigate the effect and molecular mechanism of grifolin on the proliferation, transfer, and infiltration of lung cancer (LC) cells. A control group, low grifolin group, midium grifolin group and high grifolin group, anti-miRNA-NC group, anti-miRNA-1251-5p group, grifolin + miRNA-NC group, and grifolin + miRNA-1251-5p group were established based on LC A549 cells. MTT was employed to detect cellular proliferation inhibition rate; Transwell assay was used to detect cellular transfer and infiltration; Western blot was used to test Cyclin D1, cyclin-dependent kinase inhibitor 1A (p21), matrix metalloproteinase 2 (MMP-2), and matrix metalloproteinase 9 (MMP-9) protein expression; and finally RT-qPCR was employed to test miRNA-1251-5p expression. After treatment with different concentrations of grifolin, an increase in proliferation inhibition rate of A549 cells, a decrease in migrating and invading cells, a decrease in CyclinD1, MMP-2, and MMP-9 expression, an increase in p21 expression, and a decrease in miRNA-1251-5p expression in a manner of concentration dependence was observed (P < 0.05). Inhibiting miRNA-1251-5p expression led to an increase in cellular proliferation inhibition rate, a decrease in migrating and invading cells, a decrease in CyclinD1, MMP-2, and MMP-9 expression, and an increase in p21 expression (P < 0.05). Overexpression of miRNA-1251-5p reversed the inhibitory influence of grifolin on the proliferation, transfer, and infiltration of A549 cells. Grifolin likely inhibits the proliferation, transfer, and infiltration of LC A549 cells by down-regulating miRNA-1251-5p.
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Ramirez, Pablo A., Michael P. Rettig, Matthew Holt, and John F. DiPersio. "M2-10B4 Mesenchymal Stromal Cells Confer an In Vitro Protective Effect of Murine mCGPR/+ Acute Promyelocytic Leukemic Cells Against Chemotherapy." Blood 110, no. 11 (November 16, 2007): 2844. http://dx.doi.org/10.1182/blood.v110.11.2844.2844.
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Abstract Background: The mechanisms by which AML cells and other hematologic malignancies interact with the BM microenvironment to provide a chemoprotective effect remain largely unknown. Our hypothesis is that resistance and relapse of AML may be related to altered AML-BM niche interactions, and that interruption of these interactions might enhance chemosensitivity thus overcoming chemotherapy resistance. In the current studies we have generated an in vitro model of chemotherapy protection mediated by a bone marrow (BM) stromal cell line and attempted to determine soluble and cell associated factors that mediate this protection against genotoxic stresses such as chemotherapy.sought to answer if murine stromal cells provide chemoprotection to mCGPR/+ APL cells in vitro. Methods: APL cells generated from mice in which a single copy of the human PML-RARa was knocked into the murine cathepsin G locus (mCGPR/+; Westervelt et al, Blood. 2003 Sep 1;102(5):1857-65) were cultured in 12-well plates (normal or 0.4 μm pore transwell) with or without murine M2-10B4 stromal cells. After 24 h, APL cells were left untreated or treated with AraC (40 mg/ml) or daunorubicin (DNR; 40 ng/ml) for 2 days. FACS was used to test APL cell viability, cell cycle status, and proliferation kinetics using annexin V/PI, acridine orange, and CFSE assays, respectively. Results: We observed a significant survival benefit for mCGPR/+ APL cells co-cultured with M2-10B4 stromal cells (Table 1). This survival advantage was observed in both the absence (untreated) and presence of chemotherapeutic agents. Optimal protection against both chemotherapy agents (95% daunorubicin and 92% Ara-C) was seen when APL cells were in direct contact with stromal cells. Interestingly, the survival benefit afforded by the stromal cells was largely maintained following separation of the APL cells from the M20-10B4 cells by a 0.4 um transwell (Table 1). This observation suggests that the anti-apoptotic stimulus provided by the M2-10B4 cells was mediated, at least in part, by a soluble factor released from the stromal cells. To begin to identify candidate molecules that might mediate this anti-apoptotic effect, we harvested media from wells incubated 72 h in the presence or absence of M2-10B4 cells and measured the levels of 64 different molecules using a luminex bead assay. The five abundant molecules detected in this initial screen were VCAM-1 (22-fold), SCF (29-fold), VEGF (747-fold), MCP-1 (979-fold), and MCP-3 (907-fold). It should be noted that the APL binding to stroma was not associated with alterations of cell cycle (except increase in G1a) nor decreased proliferation kinetics (no change in CFSE striping profiles relative to untreated cells). Conclusion: These results demonstrate that murine stromal cells confer a chemotherapy survival advantage for mCGPR/+ APL cells in vitro. Furthermore, antibodies and small molecules (such as mobilizing agents) that interrupt direct binding of leukemic cells to the BM microenvironment or block signaling pathways mediated by physical attachment or anti-apoptotic soluble stromal factors may be rationally used to sensitize leukemia cells to chemotherapy in vivo. Table 1. M2-10B4 stromal cells provide a survival advantage to mCG PR/+ APL cells % Apoptotic cells(AnnexinV+/PI-) Untreated Ara-C (40ng/mL) DNR (40ng/mL) No stroma 27% (SD 1.3) 80.6% (SD 1.9) 80% (SD 2.2) Transwell 4.3% (SD 4.1) 12.2% (SD 0.2) 10.1% (SD 2.8) Stroma 3.3% (SD 0.9) 8.2% (SD 0.9) 5.3% (SD 0.3)
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Capitano, Maegan L., Nirit Mor-Vaknin, Maureen Legendre, David Markovitz, and Hal E. Broxmeyer. "Extracellular DEK Is a Novel Chemotactic Agent of Lineage Negative, Sca-1 Positive, c-Kit Positive Bone Marrow Cells." Blood 124, no. 21 (December 6, 2014): 1583. http://dx.doi.org/10.1182/blood.v124.21.1583.1583.
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Abstract DEK, a nuclear DNA-binding protein that has been implicated in the regulation of transcription, chromatin architecture, and mRNA processing, is known to be secreted by macrophages and act as a proinflammatory molecule (Mor-Vanknin et al., 2006, Mol. Cell. Bio., 26: 9484). Recombinant (r)DEK is known to function as a chemotactic factor that attracts neutrophils, CD8+ T lymphocytes and natural killer cells. Few cytokines are known to be chemoattractants for hematopoietic stem (HSC) and progenitor (HPC) cells, SDF-1 being the most potent of proteins with this capability. To test whether rDEK can serve as a chemotactic agent, transwell assays were performed utilizing lineage negative, sca-1 positive, c-kit positive (LSK) mouse bone marrow and neutrophils (Ly6G+ cells) as a positive control. Both SDF-1 and DEK induced migration of LSK cells at a dose of 100ng/mL, with no significant migration occurring towards 100ng/mL of IL-8 or MIP-2. All four cytokines induced migration of Ly6G+ cells. After examining the ability of LSK cells to migrate towards various doses of rDEK (0-200ng/mL), it was determined that LSK cells can migrate towards rDEK in a dose dependent manner with the maximum chemoattraction potential (~20%) occurring at a dose of DEK equal to or greater than 50ng/mL. A checkerboard assay using LSK cells was performed to determine whether rDEK acted more as a chemotactic (directed cell movement) or a chemokinetic (random migration) agent. Checkerboard analysis demonstrated that DEK acted as a chemotactic molecule. Upon our discovery that the DEK protein has a Glu-Leu-Arg (ELR) motif, similar to that of CXC chemokines such as IL-8, we hypothesized that DEK may manifest at least some of its actions through CXCR2, known to bind and mediate the actions of IL-8 and MIP-2. In order to examine if this is indeed the case we first confirmed expression of CXCR2 on the surface of HSC and HPC. Next, to determine if LSK migration towards DEK is dependent upon its ability to signal through CXCR2, LSK cells were pretreated with a neutralizing monoclonal antibody for CXCR2 immediately prior to being placed in a transwell chemotaxis assay utilizing 100ng/mL of rDEK in the bottom chamber. Neutralizing anti-CXCR2 antibodies inhibited migration of LSK and Ly6G+ cells toward DEK; however, if LSK cells were pretreated with an isotype control or a neutralizing antibody towards CXCR4, migration towards DEK still occurred. To confirm that the neutralizing CXCR2 antibody did not inhibit migration in a non-specific manner, transwell assays were performed examining LSK migration towards SDF-1, IL-8, and MIP-2. LSK cells were still able to migrate towards SDF-1 except when CXCR4 was neutralized. No migration was observed when IL-8 or MIP-2 was utilized. When Ly6G+ cells were used CXCR2 neutralizing antibodies blocked the migration of Ly6G+ cells towards DEK, IL-8 and MIP-2. Neutralizing CXCR4 only blocked Ly6G+ migration towards SDF-1. CXCR2 is known to be a G protein-coupled receptor and this interaction can be blocked through the use of pertussis toxin which prevents G proteins from interacting with G protein-coupled receptors thus interfering with receptor signaling. Pretreatment of LSK cells with pertussis toxin significantly inhibited the migration of LSK cells towards DEK and SDF-1. These data suggest that DEK acts as a chemotactic agent for HSC and HPC in vitro. Thus, DEK may be involved in migration and homing of HSCs and HPCs. Disclosures No relevant conflicts of interest to declare.
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Zhu, Guangying, Xiongtao Yang, Wang Guohui, and Jing You. "Cancer-IgG upregulation of radioresistance in non-small cell lung cancer patients and cell lines." Journal of Clinical Oncology 38, no. 15_suppl (May 20, 2020): e21013-e21013. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e21013.
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e21013 Background: Immunoglobulin G (IgG) is produced by B lymphocytes which is an important effector molecule of human immunity. However,our collaborators in China Peking University have found that malignant tumor cells can also express IgG (cancer-IgG). This study was designed to investigate the relationship between cancer-IgG and radiosensitivity and to explore its possible mechanisms in NSCLC. Methods: First, the expression of IGHG1 (immunoglobulin heavy constant gamma 1, IGHG1) and cancer-IgG in NSCLC and their relationship with clinicopathological features and prognosis were analyzed by TCGA(The Cancer Genome Atlas, TCGA), GEO(Gene Expression Omnibus, GEO) databases and immunohistochemistry. Secondly, after silencing the expression of cancer-IgG, cell scratch test, transwell, clone formation and apoptosis experiments were performed to observe the changes of EMT and radiation sensitivity of tumor cells after irradiation. Finally, the key proteins of PI3K/Akt signaling pathway and EMT-related proteins were detected by western blot and real-time PCR. Results: 1. The expression levels of IGHG1 and cancer-IgG in NSCLC were significantly higher than those in normal lung tissues, and high expression of IGHG1 and cancer-IgG were factors of poor prognosis. And cancer-IgG was closely related to clinical stage (P = 0.042), T stage (P = 0.044) and metastasis (P = 0.007). 2. Cell scratches and transwell experiments showed that the cell migration and invasion ability of si-control+IR group were significantly enhanced, but in si-Cancer-IgG+IR group were significantly lower than si-control+IR group. 3. Cloning formation experiments showed that the number of cell clones formed in the si-cancer-IgG group was significantly less than that in the control group under 2-6 Gy irradiation. Apoptosis results showed that the apoptosis rates of si-control group, si-Cancer-IgG group, si-control+IR group and si-Cancer-IgG group were 6.36±1.69%, 21.33±1.21%, 23.31±0.96% and 52.69±2.33% respectively. The apoptotic cells in the Si-cancer-IgG group were significantly more than the si-control group. (P < 0.01). 4. Western blot results showed that p-AKT, p-GSK3β, bcl2 and Vimentin were significantly decreased in si-Cancer-IgG+IR group compared with si-control+IR, and the expression levels of BAD and E-cadherin were increased. Conclusions: Cancer-IgG may mediate radiation-induced EMT and radiotherapy resistance through the PI3K/AKT pathway.
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She, Yang, Aiyou Mao, Feng Li, and Xiaobin Wei. "P5CR1 protein expression and the effect of gene-silencing on lung adenocarcinoma." PeerJ 7 (May 14, 2019): e6934. http://dx.doi.org/10.7717/peerj.6934.
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The present study aimed to investigate the expression of pyrroline-5-carboxylate reductase 1 (P5CR1) protein in lung adenocarcinoma and paracancerous tissues and to explore the effect of silencing the encoding gene PYCR1 on the proliferation, migration, invasion, and cisplatin sensitivity in lung adenocarcinoma cells, thereby providing a novel therapeutic target for the treatment of the disease. Immunohistochemistry staining was used to detect the P5CR1 protein expression in lung adenocarcinoma and paracancerous tissues, and statistical analysis evaluated the correlation between P5CR1 protein expression and gender, age, tissue part, or pathological grade. The CCK8 assay was performed to detect the proliferation and cisplatin sensitivity, while the effect of PYCR1 on the migration and invasion of lung adenocarcinoma cells was detected by scratch test and transwell chamber assay. The findings demonstrated that the P5CR1 protein expression was significantly elevated in lung adenocarcinoma tissues and correlated with the pathological grade, whereas no significant correlation was established between the protein expression and gender, age, or tissue part. Furthermore, after PYCR1 gene silencing, the proliferation and invasion were significantly suppressed, while the sensitivity to cisplatin was significantly enhanced. Therefore, it can be speculated that the PYCR1 gene affects the biological behavior of lung adenocarcinoma and cisplatin resistance, serving as a potential therapeutic target for lung adenocarcinoma.
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Xu, Yuanying, and Meiyan Liu. "MicroRNA-1323 downregulation promotes migration and invasion of breast cancer cells by targeting tumour protein D52." Journal of Biochemistry 168, no. 1 (March 25, 2020): 83–91. http://dx.doi.org/10.1093/jb/mvaa035.
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Abstract Breast cancer (BC) is one of the most common malignancies globally in women, with high mortality rate as a result of tumour metastasis. MicroRNAs play vital roles in the occurrence and development of human cancer. This study aimed to investigate the biological roles of miR-1323 in BC. The expression levels of miR-1323 were detected by quantitative real-time PCR assay. The effect of miR-1323 on BC cell proliferation was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assay. Wound healing analysis and Matrigel Transwell assay were conducted to evaluate miR-1323-mediated BC cell migration and invasion. A luciferase reporter assay was used to test the target of miR-1323. We found that miR-1323 levels were downregulated in BC tissues and serums. Low-miR-1323 levels were associated with lymph node metastasis and advanced clinical stage. Tumour protein D52 (TPD52) was identified as a direct target of miR-1323. Low expression of miR-1323 contributed to the overexpression of TPD52 leading to enhanced BC progression. Our findings suggest that silencing of miR-1323 enhances BC development by regulating TPD52 expression, suggesting that miR-1323 and TPD52 may serve as potential therapeutic targets for BC treatment.
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Chen, Rong, Yuan Cheng, Youyi Zhang, Zijian Li, and Li Geng. "RhoC Mediates Invasion and Migration of CaSki Cells Through the Rho-Associated Serine-Threonine Protein Kinase 1 Signaling Pathway." International Journal of Gynecologic Cancer 24, no. 2 (February 2014): 184–91. http://dx.doi.org/10.1097/igc.0000000000000053.
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ObjectiveThe small GTPase RhoC in human cancers is up-regulated and correlated with tumor metastasis. However, the role of Rho/Rho-associated serine-threonine protein kinase 1 (ROCK1) signaling pathway in human cervical cancer is still unclear. In this study, we examine the effects of RhoC and its major downstream target, ROCK1, on the invasion and migration of CaSki cells to investigate the role of RhoC/ROCK1 signaling pathway in the progression of cervical squamous cell carcinoma.MethodsRhoC and ROCK1 protein expression in CaSki cells was detected by Western blotting. Scratch and transwell assays were carried out to assess the effects of RhoC on invasion and migration of CaSki cells. Cell viability was assayed by MTT test after adding the ROCK1 inhibitor Y-27632 to CaSki cells.ResultsOverexpression of RhoC protein in CaSki cells significantly increases ROCK1 expression and promotes cell invasion and migration compared with the control group (P< 0.05). However, in the inhibition of ROCK1 with Y-27632 in CaSki cells when RhoC was overexpressed, the rate of invasiveness and migration was reduced remarkably (P< 0.05), dropping to comparable levels as the control.ConclusionsThis study suggested that the activation of RhoC/ROCK1 signaling pathways is likely involved in the progression of cervical squamous cell carcinoma.
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Ma, Nai-Xia, Wei Sun, Jian Wu, Shen-Lin Liu, Lei Weng, Yang-Qing Liu, Wen-Xiu Pu, et al. "Compound Wumei Powder Inhibits the Invasion and Metastasis of Gastric Cancer via Cox-2/PGE2-PI3K/AKT/GSK3β/β-Catenin Signaling Pathway." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–16. http://dx.doi.org/10.1155/2017/3039450.
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To explore the role of CWP in invasion and migration of gastric cancer cells and its underlying molecular mechanism, we performed the experiment in SGC-7901 cells both in vitro and in vivo. In the cell experiment, we evaluated cell proliferation by MTT assay. The results showed that CWP can inhibit the growth of SGC-7901 cells. The influence on cell migration and invasion was detected by wound-healing and Transwell invasion assays. The results showed that the abilities of invasion and migration are restrained in CWP group. Western blot showed that CWP can decrease the expression of Cox-2 and inhibit the PI3K/AKT/GSK3β/β-catenin signaling pathway. In the animal experiment, we observed that CWP had an inhibitory effect on the growth of xenograft tumors of nude mice. IHC assay, ELISA, RT-PCR assay, and Western blot assay were used to test relevant cytokines of Cox-2/PGE2-PI3K/AKT/GSK3β/β-catenin pathway. The results showed that CWP can suppress relevant cytokines of Cox-2/PGE2-PI3K/AKT/GSK3β/β-catenin pathway. In conclusion, we suggest that CWP inhibits the invasion and metastasis of SGC-7901 cells via Cox-2/PGE2-PI3K/AKT/GSK3β/β-catenin signaling pathway.
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Lu, Yiping, Fangwei Liu, Chao Li, Ying Chen, Dong Weng, and Jie Chen. "IL-10-Producing B Cells Suppress Effector T Cells Activation and Promote Regulatory T Cells in Crystalline Silica-Induced Inflammatory Response In Vitro." Mediators of Inflammation 2017 (2017): 1–11. http://dx.doi.org/10.1155/2017/8415094.
Full textAbstract:
Long-term exposure to crystalline silica leads to silicosis, which is characterized by persistent lung inflammation and lung fibrosis. Multiple immune cells have been demonstrated to participate in crystalline silica-induced immune responses. Our previous study indicated that B10 could control lung inflammation through modulating the Th balance in experimental silicosis in mice. However, the regulatory mechanism of B10 on CD4+ T cells is still unclear. MACS-sorted CD19+ B cells from the three different groups were cultured with CD4+ T cells either with or without transwell insert plates to evaluate the effects of B10 on CD4+ T cells, including Teff and Treg. B10 was eliminated by anti-CD22 application in vivo. Flow cytometry was used to test the frequencies of CD4+ T cells, and the expressions of the related cytokines were detected by real-time PCR and CBA. Insufficient B10 elevated the levels of proinflammatory cytokines and promoted Th responses in a way independent upon cell-cell contact in the Teff and B cell coculture system. B10 could both increase Treg activity and enhance conversion of Teff into Treg. Our findings demonstrated that B10 could affect Th responses by the release of IL-10, enhancing Treg functions and converting Teff into Treg.
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Wang, Tao, Yang Cai, Wen Song, Ruibao Chen, Dunmei Hu, Jianhan Ye, Lu Liu, et al. "Ethyl Acetate Extracts of Semen Impatientis Inhibit Proliferation and Induce Apoptosis of Human Prostate Cancer Cell Lines through AKT/ERK Pathways." BioMed Research International 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/1243515.
Full textAbstract:
Objective. To investigate the inhibitory effect of ethyl acetate extracts of Impatiens balsamina L. on prostate cancer cells. Methods. Impatiens balsamina L. was extracted to get water, ethanol, oil ether, ethyl acetate, and butanol extracts. CCK-8 assay was used to detect the inhibitory effect. Apoptosis rates and cell cycle distribution were detected by flow cytometry. Transwell assay was performed to test the ability of migration. The expressions of Bcl-2, Bax, cleaved-caspase-3, p-ERK, ERK, p-AKT, AKT, cyclin D1, cyclin E, and MMP2 were detected by Western blot. Results. Ethyl acetate extracts had the strongest inhibitory effect. After being treated with different concentrations of ethyl acetate extracts, the percentage of G0/G1 phase increased significantly, cyclin D1 and cyclin E expression decreased, apoptosis rate was significantly higher, and the ability of migration of PC-3 and RV1 was inhibited significantly. Western blot showed that the expressions of Bcl-2, p-ERK, and p-AKT were significantly decreased, but the expressions of Bax and caspase-3 cleavage were increased. Conclusions. Impatiens balsamina L. inhibited the proliferation of human prostate cancer cells; ethyl acetate extracts have the strongest effect. It could inhibit cell proliferation and migration, cause G1 phase arrest, and induce apoptosis probably through inhibition of the AKT and ERK pathways.