Статті в журналах: "Cancer cell physiology"

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Gao, Sumei, Xiaoyan Li, Xia Ding, Wenwen Qi, and Qifeng Yang. "Cepharanthine Induces Autophagy, Apoptosis and Cell Cycle Arrest in Breast Cancer Cells." Cellular Physiology and Biochemistry 41, no. 4 (2017): 1633–48. http://dx.doi.org/10.1159/000471234.

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Background: Cepharanthine (CEP) is a biscoclaurine alkaloid extracted from Stephania cepharantha and has been shown to have an anti-tumour effect on different types of cancers. However, the anti-cancer effect of CEP on human breast cancer cells is still unclear. Methods: We used MTT, clone formation, in vitro scratch, invasion and migration assays to confirm the inhibitory role of CEP on the proliferation of breast cancer cells. Flow cytometry, plasmid construction and western blot analysis were used to study the detailed mechanisms. Results: Our study showed that CEP could inhibit cell proliferation by inducing autophagy, apoptosis, and G0/G1 cell cycle arrest of breast cancer cells. Furthermore, we found that CEP induced autophagy and apoptosis by inhibiting the AKT/mTOR signalling pathway. Conclusion: We found that CEP could inhibit growth and motility of MCF-7 and MDA-MB-231 breast cancer cell. Our study revealed an anti-tumour effect of CEP on breast cancer cells and suggests that CEP could be a potential new clinical therapy for breast cancer.

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Wang, Zhongli, and Chao Liu. "Lgr5-Positive Cells are Cancer-Stem-Cell-Like Cells in Gastric Cancer." Cellular Physiology and Biochemistry 36, no. 6 (2015): 2447–55. http://dx.doi.org/10.1159/000430205.

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Background/Aims: Effective treatment of gastric cancer (GC) requires better understanding of the molecular regulation of its carcinogenesis. Identification of cancer stem cells (CSCs) in GC appears to be a critical question. Methods: We analyzed Lgr5 expression in GC specimen. We used an adeno-associated virus (AAV) that carries diphtheria toxin fragment A (DTA) under the control of Lgr5 promoter (AAV-pLgr5-DTA) to transduce human GC cells. The growth of GC cells with/without depletion of Lgr5-positive cells was studied in vitro in an MTT assay, and in vivo by analyzing bioluminescence levels. Results: A portion of GC cells in the resected specimen expressed Lgr5. GC cells that formed tumor spheres expressed high Lgr5. Selective depletion of Lgr5-positive GC cells resulted in significant growth inhibition of GC cells in vitro and in vivo. Conclusion: Lgr5-positive cells may be CSCs-like cells in GC and may play a pivotal role in the tumorigenesis of GC. Treating Lgr5-positive GC cells may substantially improve the therapeutic outcome.

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Yin, Yu-Chun, Chao-Cheng Lin, Tzu-Ting Chen, Jen-Yeu Chen, Hui-Ju Tsai, Chia-Yu Wang, and Shiow-Yi Chen. "Clozapine Induces Autophagic Cell Death in Non-Small Cell Lung Cancer Cells." Cellular Physiology and Biochemistry 35, no. 3 (2015): 945–56. http://dx.doi.org/10.1159/000369751.

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Background/Aims: Previous studies have shown that patients with schizophrenia have a lower incidence of cancer than the general population, and several antipsychotics have been demonstrated to have cytotoxic effects on cancer cells. However, the mechanisms underlying these results remain unclear. The present study aimed to investigate the effect of clozapine, which is often used to treat patients with refractory schizophrenia, on the growth of non-small cell lung carcinoma cell lines and to examine whether autophagy contributes to its effects. Methods: A549 and H1299 cells were treated with clozapine, and cell cytotoxicity, cell cycle and autophagy were then assessed. The autophagy inhibitor bafilomycin A1 and siRNA-targeted Atg7 were used to determine the role of autophagy in the effect of clozapine. Results: Clozapine inhibited A549 and H1299 proliferation and increased p21 and p27 expression levels, leading to cell cycle arrest. Clozapine also induced a high level of autophagy, but not apoptosis, in both cell lines, and the growth inhibitory effect of clozapine was blunted by treatment with the autophagy inhibitor bafilomycin A1 or with an siRNA targeting atg7. Conclusions: Clozapine inhibits cell proliferation by inducing autophagic cell death in two non-small cell lung carcinoma cell lines. These findings may provide insights into the relationship between clozapine use and the lower incidence of lung cancer among patients with schizophrenia.

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Luo, Hua-Rong, Ying Liu, Xiao-Dong Wan, Jun-Liang Li, Min Wu, Qi-Min Zhang, Deng-Long Wu, Xin Zhao, and Tian-Ru Wang. "Sumoylation Negatively Regulates CSR1-Dependent Prostate Cancer Cell Death." Cellular Physiology and Biochemistry 46, no. 5 (2018): 1861–67. http://dx.doi.org/10.1159/000489370.

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Background/Aims: SUMOylation is a dynamic process and reversed by the activity of SUMO-specific proteases (SENPs) family. SENP1, a member of this family, is highly expressed and plays oncogenic roles in diverse cancers including prostate cancer. However, the SENP1-transgenic mice exhibit aberrant transformation of the mouse prostate gland but do not develop cancer. Cellular Stress Response 1 (CSR1) is a tumor suppressor gene and frequently deleted in prostate cancers. Overexpression of CSR1 in prostate cancer cells inhibits colony formation, anchorage-independent growth and induces cell death. Methods: The relationship between CSR1 and SENP1 were determined by immunoprecipitation-based proteomics screen and verified by GST-pull down assay. In vivo SUMOylation assay was used to detect the direct effect of SENP1 in the regulation of CSR1. Clustered regularly interspaced short palindromic repeats (CRISPR)–based gene editing was used to generate Senp1–/– and CSR1–/– PC3 cells. FACS assay was used to determine the apoptosis ratio of cells after transfection. Results: CSR1 is SUMOylated at K582 and rapid ubiquitinated and degradated in prostate cancer cells. SENP1 interacts with and deSUMOylates CSR1 to prevent its degradation and enhances CSR1-dependent prostate cancer cell death. Conclusion: Thus, our data indicates that CSR1 is a critical SUMOylated substrate of SENP1 that might partially explain the controversial roles of SENP1 in prostate cancer development.

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Cheng, Kunrong, Roxana Samimi, Guofeng Xie, Jasleen Shant, Cinthia Drachenberg, Mark Wade, Richard J. Davis, George Nomikos, and Jean-Pierre Raufman. "Acetylcholine release by human colon cancer cells mediates autocrine stimulation of cell proliferation." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 3 (September 2008): G591—G597. http://dx.doi.org/10.1152/ajpgi.00055.2008.

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Most colon cancers overexpress M3 muscarinic receptors (M3R), and post-M3R signaling stimulates human colon cancer cell proliferation. Acetylcholine (ACh), a muscarinic receptor ligand traditionally regarded as a neurotransmitter, may be produced by nonneuronal cells. We hypothesized that ACh release by human colon cancer cells results in autocrine stimulation of proliferation. H508 human colon cancer cells, which have robust M3R expression, were used to examine effects of muscarinic receptor antagonists, acetylcholinesterase inhibitors, and choline transport inhibitors on cell proliferation. A nonselective muscarinic receptor antagonist (atropine), a selective M3R antagonist ( p-fluorohexahydro-sila-difenidol hydrochloride), and a choline transport inhibitor (hemicholinum-3) all inhibited unstimulated H508 colon cancer cell proliferation by ∼40% ( P < 0.005). In contrast, two acetylcholinesterase inhibitors (eserine-hemisulfate and bis-9-amino-1,2,3,4-tetrahydroacridine) increased proliferation by 2.5- and 2-fold, respectively ( P < 0.005). By using quantitative real-time PCR, expression of choline acetyltransferase (ChAT), a critical enzyme for ACh synthesis, was identified in H508, WiDr, and Caco-2 colon cancer cells. By using high-performance liquid chromatography-electrochemical detection, released ACh was detected in H508 and Caco-2 cell culture media. Immunohistochemistry in surgical specimens revealed weak or no cytoplasmic staining for ChAT in normal colon enterocytes ( n = 25) whereas half of colon cancer specimens ( n = 24) exhibited moderate to strong staining ( P < 0.005). We conclude that ACh is an autocrine growth factor in colon cancer. Mechanisms that regulate colon epithelial cell production and release of ACh warrant further investigation.

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Bose, Shree, Vijyendra Ramesh, and Jason W. Locasale. "Acetate Metabolism in Physiology, Cancer, and Beyond." Trends in Cell Biology 29, no. 9 (September 2019): 695–703. http://dx.doi.org/10.1016/j.tcb.2019.05.005.

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Liu, Shunli, Mingrui Chen, Pengcheng Li, Yujia Wu, Chunjuan Chang, Yabin Qiu, Ling Cao, Zhen Liu, and Chiyu Jia. "Ginsenoside Rh2 Inhibits Cancer Stem-Like Cells in Skin Squamous Cell Carcinoma." Cellular Physiology and Biochemistry 36, no. 2 (2015): 499–508. http://dx.doi.org/10.1159/000430115.

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Background/Aims: Treatments targeting cancer stem cells (CSCs) are most effective cancer therapy, whereas determination of CSCs is challenging. We have recently reported that Lgr5-positive cells are cancer stem cells (CSCs) in human skin squamous cell carcinoma (SCC). Ginsenoside Rh2 (GRh2) has been shown to significantly inhibit growth of some types of cancers, whereas its effects on the SCC have not been examined. Methods: Here, we transduced human SCC cells with lentivirus carrying GFP reporter under Lgr5 promoter. The transduced SCC cells were treated with different doses of GRh2, and then analyzed cell viability by CCK-8 assay and MTT assay. The effects of GRh2 on Lgr5-positive CSCs were determined by fow cytometry and by tumor sphere formation. Autophagy-associated protein and β-catenin were measured by Western blot. Expression of short hairpin small interfering RNA (shRNA) for Atg7 and β-catenin were used to inhibit autophagy and β-catenin signaling pathway, respectively, as loss-of-function experiments. Results: We found that GRh2 dose-dependently reduced SCC viability, possibly through reduced the number of Lgr5-positive CSCs. GRh2 increased autophagy and reduced β-catenin signaling in SCC cells. Inhibition of autophagy abolished the effects of GRh2 on β-catenin and cell viability, while increasing β-catenin abolished the effects of GRh2 on autophagy and cell viability. Conclusion: Taken together, our data suggest that GRh2 inhibited SCC growth, possibly through reduced the number of Lgr5-positive CSCs. This may be conducted through an interaction between autophagy and β-catenin signaling.

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Bai, Xiaoxue, Lin Meng, Huijie Sun, Zhuo Li, Xiufang Zhang, and Shucheng Hua. "MicroRNA-196b Inhibits Cell Growth and Metastasis of Lung Cancer Cells by Targeting Runx2." Cellular Physiology and Biochemistry 43, no. 2 (2017): 757–67. http://dx.doi.org/10.1159/000481559.

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Background/Aims: Lung cancer is one of the most common causes of cancer related deaths worldwide. The role of several microRNAs (miRNAs) including miR-196b in different cancers has already been established. The study was aimed to explore the role of miR-196b in lung cancer and its possible underlying mechanism. Methods: Human lung cancer cell line A549 was transfected with miR-196b mimic, miR-196b inhibitor and corresponding controls. Then cell viability, migration, invasion, and apoptosis of A549 lung cancer cells either with overexpression or with suppression of miR-196b were estimated sequentially. Next, dual luciferase activity assay was performed to clarify whether Runx2 was a direct target of miR-196b. Finally, the expressions of main factors associated with epithelial mesenchymal transition (EMT), PI3K/AKT/GSK3β, Smad, and JNK pathways were detected by western blot. Results: MiR-196b expression was significantly decreased in A549, H1650 and H1299 cell lines compared with in WI-38 and HEL-1 cell lines. Overexpression of miR-196b suppressed cell viability, migration, invasion, and induced apoptosis as well as inhibited TGF-β induced EMT process in A549 cells. In addition, Runx2 was a putative target of miR-196b, and Runx2 silence remarkably increased cell apoptosis and abolished the promotive effects of miR-196b suppression on cell viability, migration and invasion. Finally, miR-196b also mediated its action by inactivation of PI3K/AKT/GSK3β, Smad, and JNK pathways by down-regulation of Runx2. Conclusion: MiR-196b functions as a tumor suppressor that inhibited cell growth and metastasis of lung cancer cells by targeting Runx2. These findings provided further evidences for treatment of lung cancer.

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Gao, Zhuo, Ruiqi Liu, Na Ye, Chao Liu, Xiuli Li, Xiaodong Guo, Zhuoran Zhang, Xiaoxi Li, Yuanfei Yao, and Xiaofeng Jiang. "FOXO1 Inhibits Tumor Cell Migration via Regulating Cell Surface Morphology in Non-Small Cell Lung Cancer Cells." Cellular Physiology and Biochemistry 48, no. 1 (2018): 138–48. http://dx.doi.org/10.1159/000491670.

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Background/Aims: Cell surface morphology plays pivotal roles in malignant progression and epithelial-mesenchymal transition (EMT). Previous research demonstrated that microvilli play a key role in cell migration of non-small cell lung cancer (NSCLC). In this study, we report that Forkhead box class O1 (FOXO1) is downregulated in human NSCLC and that silencing of FOXO1 is associated with the invasive stage of tumor progression. Methods: The cell proliferation, migration, and invasion were characterized in vitro, and we tested the expression of the Epithelial-mesenchymal transition (EMT) marker by immunofluorescence staining and also identified the effect of FOXO1 on the microvilli by scanning electron microscopy (SEM). Results: Functional analyses revealed that silencing of FOXO1 resulted in an increase in NSCLC cell proliferation, migration, and invasion; whereas overexpression of FOXO1 significantly inhibited the migration and invasive capability of NSCLC cells in vitro. Furthermore, cell morphology imaging showed that FOXO1 maintained the characteristics of epithelial cells. Immunofluorescence staining and western blotting showed that the E-cadherin level was elevated and Vimentin was reduced by FOXO1 overexpression. Conversely, the E-cadherin level was reduced and Vimentin was elevated in cells silenced for FOXO1. Furthermore, scanning electron microscopy (SEM) showed that FOXO1 overexpression increased the length of the microvilli on the cell surface, whereas FOXO1 silencing significantly reduced their length. Conclusions: FOXO1 is involved in human lung carcinogenesis and may serve as a potential therapeutic target in the migration of human lung cancer.

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Arcangeli, Annarosa, and Jason X. J. Yuan. "American Journal of Physiology-Cell Physiology theme: ion channels and transporters in cancer." American Journal of Physiology-Cell Physiology 301, no. 2 (August 2011): C253—C254. http://dx.doi.org/10.1152/ajpcell.00159.2011.

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Zhu, Ying, Chaoxiong Zhang, Changxin Gu, Qiang Li, and Ning Wu. "Function of Deubiquitinating Enzyme USP14 as Oncogene in Different Types of Cancer." Cellular Physiology and Biochemistry 38, no. 3 (2016): 993–1002. http://dx.doi.org/10.1159/000443051.

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Background/Aims: Non-small cell lung cancer (NSCLC) tissues overexpress USP14, which promotes tumor cell proliferation and is associated with shorter overall survival time. Methods: The expression of USP14 was assayed in many types of cancers. USP14 was up-and down-regulated using appropriate plasmid or lentiviral vector constructs and its effects on proliferation, cell colony number, and apoptosis rate were measured. A human NSCLC cell line was inoculated into nude mice and the survival rates were recorded. Results: We found USP14 amplification and overexpression in many different cancers. The overexpression of USP14 in USP14 low-expression cell lines promoted cell proliferation and migration, whereas USP14 downregulation suppressed tumor cell proliferation, decreased tumor cell colony number, increased apoptosis rate, and decreased cell migration and invasion. Conclusion: USP14 plays an oncogenic role in various types of cancer, and may thus represent a new cancer therapy target.

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Ma, Gwang Taek, Sun Kyoung Lee, Kwang-Kyun Park, Junhee Park, Seung Hwa Son, Mankil Jung, and Won-Yoon Chung. "Artemisinin-Daumone Hybrid Inhibits Cancer Cell-Mediated Osteolysis by Targeting Cancer Cells and Osteoclasts." Cellular Physiology and Biochemistry 49, no. 4 (2018): 1460–75. http://dx.doi.org/10.1159/000493449.

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Background/Aims: Bone metastasis of cancer cells decreases patient survival and quality of life. Hybridization via the covalent coupling of two bioactive natural products is a useful strategy for developing more potent anticancer agents by enhancing their bioavailability and avoiding drug resistance. Methods: The in vivo activities of artemisinin-daumone hybrid 15 (ARTD) were estimated in cancer cell-inoculated mice and ovariectomized mice. The viability, migration, and invasion of cancer cells were measured via MTT, wound-healing, and transwell invasion assays. ARTD-regulated transcription factors were detected with an RT2 profiler PCR array kit and Western blotting. Osteoclastogenesis and osteoclast activity were detected with tartrate-resistant acid phosphatase staining, a pit formation assay, gelatin zymography, and a cathepsin K ELISA assay. Results: ARTD blocked cancer-associated osteolysis more potently than artemisinin in mice with intratibially inoculated breast cancer or lung cancer cells. ARTD inhibited the viability, migration, and invasion of breast and lung cancer cells in the absence or presence of transforming growth factor-β1. ARTD treatment induced the expression of tumor suppressive activating transcription factor 3 and inhibited oncogenic E2F transcription factor 1 expression at the mRNA and protein levels. ARTD inhibited receptor activator of nuclear factor kappa-B ligand-induced osteoclast formation and bone resorbing activity by reducing the secreted levels of matrix metalloproteinase-9 and cathepsin K. Furthermore, ARTD prevented estrogen deficiency-induced bone loss in ovariectomized mice. Conclusion: ARTD may be a promising candidate for inhibiting cancer-induced bone destruction. The application of ARTD may be extended to patients with chemotherapy-induced ovarian failure or postmenopausal osteoporosis.

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Estaras, Matias, and Antonio Gonzalez. "Modulation of cell physiology under hypoxia in pancreatic cancer." World Journal of Gastroenterology 27, no. 28 (July 28, 2021): 4582–602. http://dx.doi.org/10.3748/wjg.v27.i28.4582.

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Hensley, Christopher T., Ajla T. Wasti, and Ralph J. DeBerardinis. "Glutamine and cancer: cell biology, physiology, and clinical opportunities." Journal of Clinical Investigation 123, no. 9 (September 3, 2013): 3678–84. http://dx.doi.org/10.1172/jci69600.

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Shih, Chuan-Chi, Hsiu-Chuan Chou, Ying-Jen Chen, Wen-Hung Kuo, Chia-Hao Chan, Yi-Chieh Lin, En-Chi Liao, Shing-Jyh Chang, and Hong-Lin Chan. "Role of PGRMC1 in cell physiology of cervical cancer." Life Sciences 231 (August 2019): 116541. http://dx.doi.org/10.1016/j.lfs.2019.06.016.

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Arafat, Kholoud, Elham Al Kubaisy, Shahrazad Sulaiman, Sherif M. Karam, Zeina Al Natour, Ahmed H. Hassan, and Samir Attoub. "SMARCAD1 in Breast Cancer Progression." Cellular Physiology and Biochemistry 50, no. 2 (2018): 489–500. http://dx.doi.org/10.1159/000494163.

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Background/Aims: Breast cancer is the most common cancer in women worldwide, and within this cancer type, triple-negative breast cancers have the worst prognosis. The identification of new genes associated with triple-negative breast cancer progression is crucial for developing more specific anti-cancer targeted therapies, which could lead to a better management of these patients. In this context, we have recently demonstrated that SMARCAD1, a DEAD/H box-containing helicase, is involved in breast cancer cell migration, invasion, and metastasis. The aim of this study was to investigate the impact of the stable knockdown of SMARCAD1 on human breast cancer cell progression. Methods: Using two different designs of shRNA targeting SMARCAD1, we investigated the impact of the stable knockdown of SMARCAD1 on human breast cancer cell proliferation and colony growth in vitro and on tumour growth in chick embryo and nude mouse xenograft models in vivo using MDA-MB-231 (ER-/PR-/ HER2-) and T47D (ER+/PR+/-/HER2-) human breast cancer cell lines. Results: We found that SMARCAD1 knockdown resulted in a significant decrease in breast cancer cell proliferation and colony formation, leading to the significant inhibition of tumour growth in both the chick embryo and nude mouse xenograft models. This inhibition was due, at least in part, to a decrease in IKKβ expression. Conclusion: These results indicate that SMARCAD1 is involved in breast cancer progression and can be a promising target for breast cancer therapy.

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Pozzi, Valentina, Davide Sartini, Romina Rocchetti, Andrea Santarelli, Corrado Rubini, Stefano Morganti, Rachela Giuliante, et al. "Identification and Characterization of Cancer Stem Cells from Head and Neck Squamous Cell Carcinoma Cell Lines." Cellular Physiology and Biochemistry 36, no. 2 (2015): 784–98. http://dx.doi.org/10.1159/000430138.

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Background/Aims: Head and neck squamous cell carcinoma (HNSCC) ranks sixth worldwide for tumor-related mortality. A subpopulation of tumor cells, termed cancer stem cells (CSCs), has the ability to support cancer growth. Therefore, profiling CSC-enriched populations could be a reliable tool to study cancer biology. Methods: We performed phenotypic characterization of 7 HNSCC cell lines and evaluated the presence of CSCs. CSCs from Hep-2 cell line and HNSCC primary cultures were enriched through sphere formation and sphere-forming cells have been characterized both in vitro and in vivo. In addition, we investigated the expression levels of Nicotinamide N-methyltransferase (NNMT), an enzyme overexpressed in several malignancies. Results: CSC markers were markedly expressed in Hep-2 cell line, which was found to be highly tumorigenic. CSC-enriched populations displayed increased expression of CSC markers and a strong capability to form tumors in vivo. We also found an overexpression of CSC markers in tumor formed by CSC-enriched populations. Interestingly, NNMT levels were significantly higher in CSC-enriched populations compared with parental cells. Conclusion: Our study provides an useful procedure for CSC identification and enrichment in HNSCC. Moreover, results obtained seem to suggest that CSCs may represent a promising target for an anticancer therapy.

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Titu, Stefan, Cristiana Maria Grapa, Teodora Mocan, Ovidiu Balacescu, and Alexandru Irimie. "Tetraspanins: Physiology, Colorectal Cancer Development, and Nanomediated Applications." Cancers 13, no. 22 (November 12, 2021): 5662. http://dx.doi.org/10.3390/cancers13225662.

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Tetraspanins are transmembrane proteins expressed in a multitude of cells throughout the organism. They contribute to many processes that surround cell–cell interactions and are associated with the progress of some diseases, including cancer. Their crucial role in cell physiology is often understated. Furthermore, recent studies have shown their great potential in being used as targeting molecules. Data have suggested the potential of tetraspanins as a targeting vector for nanomediated distribution and delivery for colorectal cancer applications. Our aim is to provide a review on the important part that tetraspanins play in the human organism and highlight their potential use for drug delivery systems using nanotechnology.

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Coltart, Stewart, and Catriona Irvine. "Hyperthermia, cell proliferation and cancer." International Journal of Hyperthermia 2, no. 4 (January 1986): 389–90. http://dx.doi.org/10.3109/02656738609004969.

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Riese, David J., and Richard L. Cullum. "Epiregulin: Roles in normal physiology and cancer." Seminars in Cell & Developmental Biology 28 (April 2014): 49–56. http://dx.doi.org/10.1016/j.semcdb.2014.03.005.

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Yu, Xinyi, Feng Liu, Liyi Zeng, Fang He, Ruyi Zhang, Shujuan Yan, Zongyue Zeng, et al. "Niclosamide Exhibits Potent Anticancer Activity and Synergizes with Sorafenib in Human Renal Cell Cancer Cells." Cellular Physiology and Biochemistry 47, no. 3 (2018): 957–71. http://dx.doi.org/10.1159/000490140.

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Background/Aims: As the most lethal urological cancers, renal cell carcinoma (RCC) comprises a heterogeneous group of cancer with diverse genetic and molecular alterations. There is an unmet clinical need to develop efficacious therapeutics for advanced, metastatic and/or relapsed RCC. Here, we investigate whether anthelmintic drug Niclosamide exhibits anticancer activity and synergizes with targeted therapy Sorafenib in suppressing RCC cell proliferation. Methods: Cell proliferation and migration were assessed by Crystal violet staining, WST-1 assay, cell wounding and cell cycle analysis. Gene expression was assessed by qPCR. In vivo anticancer activity was assessed in xenograft tumor model. Results: We find that Niclosamide effectively inhibits cell proliferation, cell migration and cell cycle progression, and induces apoptosis in human renal cancer cells. Mechanistically, Niclosamide inhibits the expression of C-MYC and E2F1 while inducing the expression of PTEN in RCC cells. Niclosamide is further shown to synergize with Sorafenib in suppressing RCC cell proliferation and survival. In the xenograft tumor model, Niclosamide is shown to effectively inhibit tumor growth and suppress RCC cell proliferation. Conclusions: Niclosamide may be repurposed as a potent anticancer agent, which can potentiate the anticancer activity of the other agents targeting different signaling pathways in the treatment of human RCC.

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Singh, P., Z. Xu, B. Dai, S. Rajaraman, N. Rubin, and B. Dhruva. "Incomplete processing of progastrin expressed by human colon cancer cells: role of noncarboxyamidated gastrins." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 3 (March 1, 1994): G459—G468. http://dx.doi.org/10.1152/ajpgi.1994.266.3.g459.

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Gastrin is mitogenic for several colon cancers. To assess a possible autocrine role of gastrin in colon cancers, we examined human colon cancer cell lines for expression of gastrin mRNA and various forms of gastrin. Gastrin mRNA was not detected in the majority of colon cancer cell lines by Northern hybridization but was detected in all human colon cancer lines by the sensitive method of reverse transcriptase-polymerase chain reaction (PCR). Gastrin mRNA was quantitated by the competitive PCR method. The majority of cell lines expressed very low levels of gastrin mRNA (< 1-5 copies/cell); only one cell line expressed > 20 copies/cell. The mature carboxyamidated form of gastrin was not detected in any of the cell lines by radioimmunoassay or immunocytochemistry. Results suggested that either gastrin mRNA expressed by colon cancer cells was altered (mutated) or posttranslational processing of progastrin was incomplete. Gastrin cDNA from all the colon cancer cell lines had an identical sequence to the published sequence of human gastrin cDNA. Specific antibodies against precursor forms of gastrin were used, and significant concentrations of nonamidated (glycine-extended) and prepro forms of gastrin were measured in tumor extracts of representative colon cancer cell lines. The presence of precursor forms of gastrin suggested a lack of one or more of the processing enzymes and/or cofactors. Significant concentrations of the processing enzyme (peptidylglycine alpha-amidating monooxygenase) were detected in colon cancer cells by immunocytochemistry. Therefore, lack of other cofactors or enzymes may be contributing to incomplete processing of precursor forms of gastrin, which merits further investigation. Since low levels of gastrin mRNA were expressed by the majority of human colon cancer cell lines and progastrin was incompletely processed, it seems unlikely that gastrin can function as a viable autocrine growth factor for colon cancer cells. High concentrations of glycine-extended gastrin-17 (GG) (> 10(-6) M) were mitogenic for a gastrin-responsive human colon cancer (DLD-1) cell line in vitro. It remains to be seen if GG or other precursor forms of gastrin are similarly mitogenic in vivo, which may then lend credibility to a possible autocrine role of gastrinlike peptides in colon cancers.

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Edamana, Sarannya, Frédéric H. Login, Soichiro Yamada, Tae-Hwan Kwon, and Lene N. Nejsum. "Aquaporin water channels as regulators of cell-cell adhesion proteins." American Journal of Physiology-Cell Physiology 320, no. 5 (May 1, 2021): C771—C777. http://dx.doi.org/10.1152/ajpcell.00608.2020.

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Aquaporin (AQP) water channels facilitate passive transport of water across cellular membranes following an osmotic gradient. AQPs are expressed in a multitude of epithelia, endothelia, and other cell types where they play important roles in physiology, especially in the regulation of body water homeostasis, skin hydration, and fat metabolism. AQP dysregulation is associated with many pathophysiological conditions, including nephrogenic diabetes insipidus, chronic kidney disease, and congestive heart failure. Moreover, AQPs have emerged as major players in a multitude of cancers where high expression correlates with metastasis and poor prognosis. Besides water transport, AQPs have been shown to be involved in cellular signaling, cell migration, cell proliferation, and regulation of junctional proteins involved in cell-cell adhesion; all cellular processes which are dysregulated in cancer. This review focuses on AQPs as regulators of junctional proteins involved in cell-cell adhesion.

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Chen, Yi, Ya Peng, Zhipeng Xu, Bo Ge, Xuebao Xiang, Tianyu Zhang, Li Gao, Hailin Shi, Chuang Wang, and Jiefu Huang. "LncROR Promotes Bladder Cancer Cell Proliferation, Migration, and Epithelial-Mesenchymal Transition." Cellular Physiology and Biochemistry 41, no. 6 (2017): 2399–410. http://dx.doi.org/10.1159/000475910.

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Background: LncRNA ROR, a tumor oncogene associated with various human cancers, has been reported to be involved in regulating various cellular processes, such as proliferation, apoptosis and invasion through targeting multiple genes. However, the molecular biological function in bladder cancer has not been clearly elucidated. The aim of this study is to explore ROR expression levels and evaluated its function in bladder cancer. Methods: LncRNA ROR expression levels in the 36 pairs of bladder cancer tissues (and corresponding non-tumor tissues) and bladder cancer cells were assessed by qRT-PCR. MTT assay, colony formation assay, flow cytometric analysis, wound healing assay, cell transwell assays, attachment/detachment and western blotting were performed to assess the effects of ROR on proliferation, apoptosis, migration/invasion and epithelial-to-mesenchymal (EMT) phenotypes in BC cells in vitro. ZEB1 is target of ROR. Rescue assays were performed to further confirm that ROR contributes to the progression of BC cells through targeting ZEB1. Results: LncRNA ROR was up-regulated in bladder cancer tissues (compared to adjacent non-tumor tissues) and was almost overexpression in bladder cancer cells (compared with normal urothelial cell line SVHUC-1 cells). Increased lncRNA ROR expression significantly promoted tumor cells proliferation, inhibited cells apoptosis, facilitated cells metastasis and contributed to the formation of EMT phenotype. While down-regulated ROR could obviously inhibit cells proliferation, promote cells apoptosis, inhibit metastasis and reverse EMT to MET. ZEB1 was a target gene of ROR and was positive correlation with the level of ROR in cancer tissues. Conclusion: These results indicated that lncRNA ROR was associated with tumor progression in bladder cancer cells.

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Ma, Jun, Ning Wang, Yurong Zhang, Cun Wang, Tianxiang Ge, Haojie Jin, Xuan Deng, et al. "KDM6B Elicits Cell Apoptosis by Promoting Nuclear Translocation of FOXO1 in Non-Small Cell Lung Cancer." Cellular Physiology and Biochemistry 37, no. 1 (2015): 201–13. http://dx.doi.org/10.1159/000430345.

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Background/Aims: Non-small cell lung carcinoma (NSCLC) is the most common type of lung cancer and the cause of most cancer-related deaths. The molecular mechanisms that are involved in NSCLC development are currently not well understood. Accumulating evidence shows that histone demethylases play important roles in the regulation of pathological developmental processes in many diseases, including various types of cancers. Methods: Mitochondrial membrane potential assays, migration and invasion assays, caspase-3 and caspase-9 activity assays and western blot analysis were used in this research. Results: We found that overexpression of KDM6B, a demethylase that acts on histone H3 at lysine 27 (H3K27), inhibited cell growth by initiating mitochondria-dependent apoptosis and by attenuating the invasion-metastasis cascade in NSCLC cells. Moreover, our results showed that KDM6B directly interacted with FOXO1 and that overexpression of KDM6B promoted nuclear accumulation of FOXO1. The effects of KDM6B on cell apoptosis and metastasis were weakened by knockdown of FOXO1 expression. On the contrary, knocking down expression of KDM6B inhibited cell apoptosis and promoted cell growth by mitigating the nuclear translocation of FOXO1 in NSCLC cells. Conclusions: These findings suggest that KDM6B may act in a pro-apoptotic role in NSCLC by causing the nuclear translocation of FOXO1.

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Park, Seong-Min, Eun-Young Choi, Dong-Hyuck Bae, Hyun Ahm Sohn, Seon-Young Kim, and Youn-Jae Kim. "The LncRNA EPEL Promotes Lung Cancer Cell Proliferation Through E2F Target Activation." Cellular Physiology and Biochemistry 45, no. 3 (2018): 1270–83. http://dx.doi.org/10.1159/000487460.

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Background/Aims: Recent studies have revealed that many long non-coding RNAs (lncRNAs) play oncogenic or tumor-suppressive roles in various cancers. Lung cancer is the leading cause of cancer-related death worldwide, and many lung cancer patients frequently relapse after surgery, even those in the early stages. However, the oncogenic or tumor-suppressive roles and clinical implications of lncRNAs in lung cancer have not been fully elucidated. Methods: The association between an E2F-mediated cell proliferation enhancing lncRNA (EPEL) expression and lung cancer patient survival was accessed using public microarray data with clinical information. Cancer-related phenotypes were analyzed by the siRNA knockdown of EPEL in two lung cancer cell lines. Gene set analysis of gene expression data were performed to identify pathways regulated by EPEL. RNA immunoprecipitation, RT-qPCR, and ChIP assays were performed to explore the functions of selected target genes regulated by EPEL. Results: EPEL, known as LOC90768 and MGC45800, was associated with the relapse and survival of lung cancer patients and promoted lung cancer cell proliferation through the activation of E2F target genes. EPEL knockdown specifically down-regulated the expression of cell cycle-related E2F target genes, including Cyclin B1 (CCNB1), in lung cancer cells but not that of apoptosis- or metabolism-related E2F target genes. EPEL interacted with E2F1 and regulated the expression of the E2F target genes by changing the binding efficiency of E2F1 to the E2F target promoters. Moreover, the expression levels of EPEL and CCNB1 both alone and in combination were robust prognostic markers for lung cancer. Conclusions: Considering its specific effects on cell cycle-related E2F target genes and its significant association with the prognosis of lung cancer patients, we suggest that the transcriptional regulation of EPEL through E2F target genes is potentially a target for the development of novel therapeutic strategies for lung cancer patients.

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Willier, Semjon, Elke Butt, Günther H. S. Richter, Stefan Burdach, and Thomas G. P. Grunewald. "Defining the role of TRIP6 in cell physiology and cancer." Biology of the Cell 103, no. 12 (December 2011): 573–91. http://dx.doi.org/10.1042/bc20110077.

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Preston, Thomas J., Arkan Abadi, Leigh Wilson, and G. Singh. "Mitochondrial contributions to cancer cell physiology: potential for drug development." Advanced Drug Delivery Reviews 49, no. 1-2 (July 2001): 45–61. http://dx.doi.org/10.1016/s0169-409x(01)00127-2.

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Lin, Jieping, Teng Yang, Zheng Peng, Haiyan Xiao, Na Jiang, Lifang Zhang, Dickerson CA, Ping Wu, and Qingjun Pan. "SLC1A5 Silencing Inhibits Esophageal Cancer Growth via Cell Cycle Arrest and Apoptosis." Cellular Physiology and Biochemistry 48, no. 1 (2018): 397. http://dx.doi.org/10.1159/000491769.

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Background/Aims: Solute-linked carrier family A1 member 5 (SLC1A5), which has high affinity to neutral amino acids, is essential for glutamine transport and amino acid metabolism in various cancers. However, the role of SLC1A5 in esophageal cancer has not been reported. Methods: SLC1A5 expression in esophageal cancer tissues was detected by immunohistochemistry and western blotting. The effects of SLC1A5 knockdown on the growth, cell cycle, viability, and glutamine metabolism of esophageal cancer cells were investigated with flow cytometry and western blotting. Furthermore, the consequences of SLC1A5 knockdown on tumor growth and survival were also evaluated in vivo using mice carrying esophageal cancer xenografts. Results: SLC1A5 was expressed in 86.5% (32/37) of the cancer tissues from esophageal cancer patients. Moreover, SLC1A5 expression in the cancerous tissues was significantly higher than that in the paired adjacent normal tissues. SLC1A5 knockdown with siRNA (PZ siRNA) in TE-1 cells in vitro significantly decreased cell growth and reduced both leucine and glutamine transport, leading to inhibition of mTORC1 signaling. Additionally, siRNA-mediated SLC1A5 knockdown resulted in cell cycle arrest and apoptosis of TE-1 cells. The survival rate of athymic (nu/nu) male nude mice carrying tumors formed from TE-1 cells transfected with SLC1A5 siRNA (PZ siRNA) was also significantly improved compared with mice carrying tumors formed from TE-1 cells transfected with control siRNA. Tumor size/weight was also significantly lower for the former mice group of mice. Conclusion: Our data indicate that SLC1A5 plays an important role in esophageal cancer both in vivo and in vitro. The inhibition of esophageal cancer growth by targeting SLC1A5 could, therefore, be used as a preoperative therapy for esophageal cancer.

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Ungard, Robert G., Eric P. Seidlitz, and Gurmit Singh. "Oxidative stress and cancer pain." Canadian Journal of Physiology and Pharmacology 91, no. 1 (January 2013): 31–37. http://dx.doi.org/10.1139/cjpp-2012-0298.

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Breast cancers are the most common source of metastases to bone, of which cancer-induced bone pain is a frequent pathological feature. Cancer-induced bone pain is a unique pain state with multiple determinants that remains to be well understood and managed. Current standard treatments are limited by dose-dependent side effects that can reduce the quality of life of patients. Glutamate is a neurotransmitter and bone cell-signalling molecule that is released via the system [Formula: see text] cystine/glutamate antiporter from cancer cell types that frequently metastasize to bone, including breast cancers. In cancer cells, glutamate release is understood to be a side effect of the cellular response to oxidative stress that upregulates the expression and activity of system [Formula: see text] to promote the increased import of cystine. Attenuation of glutamate release from cancer cells has been demonstrated to result in reductions in associated cancer-induced bone pain in animal models. This review examines the clinical implications of attenuating cystine uptake and glutamate release in the treatment of cancer-induced bone pain.

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Bittman, Kevin S. "Immune Cell Metabolic Fitness for Life." Antibodies 11, no. 2 (April 30, 2022): 32. http://dx.doi.org/10.3390/antib11020032.

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Adoptive cell therapy holds great promise for treating a myriad of diseases, especially cancer. Within the last decade, immunotherapy has provided a significant leap in the successful treatment of leukemia. The research conducted throughout this period to understand the interrelationships between cancer cells and infiltrating immune cells winds up having one very common feature, bioenergetics. Cancer cells and immune cells both need ATP to perform their individual functions and cancer cells have adopted means to limit immune cell activity via changes in immune cell bioenergetics that redirect immune cell behavior to encourage tumor growth. Current leading strategies for cancer treatment super-charge an individual’s own immune cells against cancer. Successful Chimeric Antigen Receptor T Cells (CAR T) target pathways that ultimately influence bioenergetics. In the last decade, scientists identified that mitochondria play a crucial role in T cell physiology. When modifying T cells to create chimeras, a unique mitochondrial fitness emerges that establishes stemness and persistence. This review highlights many of the key findings leading to this generation’s CAR T treatments and the work currently being done to advance immunotherapy, to empower not just T cells but other immune cells as well against a variety of cancers.

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Anbarasan, Thineskrishna, and Jean-Christophe Bourdon. "The Emerging Landscape of p53 Isoforms in Physiology, Cancer and Degenerative Diseases." International Journal of Molecular Sciences 20, no. 24 (December 11, 2019): 6257. http://dx.doi.org/10.3390/ijms20246257.

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p53, first described four decades ago, is now established as a master regulator of cellular stress response, the “guardian of the genome”. p53 contributes to biological robustness by behaving in a cellular-context dependent manner, influenced by several factors (e.g., cell type, active signalling pathways, the type, extent and intensity of cellular damage, cell cycle stage, nutrient availability, immune function). The p53 isoforms regulate gene transcription and protein expression in response to the stimuli so that the cell response is precisely tuned to the cell signals and cell context. Twelve isoforms of p53 have been described in humans. In this review, we explore the interactions between p53 isoforms and other proteins contributing to their established cellular functions, which can be both tumour-suppressive and oncogenic in nature. Evidence of p53 isoform in human cancers is largely based on RT-qPCR expression studies, usually investigating a particular type of isoform. Beyond p53 isoform functions in cancer, it is implicated in neurodegeneration, embryological development, progeroid phenotype, inflammatory pathology, infections and tissue regeneration, which are described in this review.

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Chang, Kuo-Ting, Chun-Ming Tsai, Yih-Chy Chiou, Chao-Hua Chiu, King-Song Jeng, and Chi-Ying F. Huang. "IL-6 induces neuroendocrine dedifferentiation and cell proliferation in non-small cell lung cancer cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 289, no. 3 (September 2005): L446—L453. http://dx.doi.org/10.1152/ajplung.00089.2005.

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Interleukin-6 (IL-6) has been identified as an important growth regulator of lung cancer cells. Elevation of serum levels of IL-6 has been found in a subpopulation of lung cancer patients, but rarely in patients with benign lung diseases. Approximately 15% of non-small cell lung cancer (NSCLC) tumors exhibit neuroendocrine (NE) properties (NSCLC-NE) and have been suggested to have the biological characteristics similar to small cell lung cancer (SCLC) with early metastasis and initial responsiveness to chemotherapy. We recently showed that IL-6 promotes cell proliferation and downregulates the expression of neuron-specific enolase (NSE, one of the major NE markers) in NSCLC-NE cells. In this study, we show that IL-6 stimulates a transient increase of tyrosine phosphorylation of STAT3 in a dose-dependent fashion. Inhibition of STAT3 signaling pathway by either AG-490 (JAK2-specific inhibitor) or overexpression of STAT3Y705F (a dominant-negative STAT3) reverses NSE expression in IL-6- treated NSCLC-NE cells. In addition, IL-6 induces phosphorylation and activation of p38 MAPK. SB-203580, a p38 MAPK-specific inhibitor, inhibits IL-6-induced p38 MAPK phosphorylating activity and suppresses IL-6-stimulated cell proliferation. Together, our results indicate that STAT3 signaling pathway is involved in IL-6-induced NE differentiation and that p38 MAPK is associated with IL-6-stimulated growth regulation in NSCLC-NE cells. These data suggest that both kinase pathways play critical roles in the pathogenesis of NSCLC-NE malignancies, providing new molecular targets for future therapeutic approaches.

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Wang, Mengying, Yayun Zhang, Taishu Wang, Jinrui Zhang, Zhu Zhou, Yan Sun, Shanshan Wang, et al. "The USP7 Inhibitor P5091 Induces Cell Death in Ovarian Cancers with Different P53 Status." Cellular Physiology and Biochemistry 43, no. 5 (2017): 1755–66. http://dx.doi.org/10.1159/000484062.

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Background/Aims: Ovarian cancer is often diagnosed at later stages with poor prognosis. Recent studies have associated the expression of deubiquitylase USP7 with the survival of ovarian cancers. Being a cysteine protease, USP7 could become a target for pharmacological intervention. Therefore, in this study, we assessed the influence of its inhibitor P5091 on ovarian cancer cells. Methods: Ovarian cancer cells were treated with P5091, and cell proliferation was measured with MTT assay; cell morphology was inspected under a phase-contrast microscope; cell cycle and cell death were examined by flow cytometry. To gain mechanistic insights into its effects, immunoblotting was performed to detect USP7, HDM2, p53, p21, apoptosis and autophagy related proteins. Results: P5091 effectively suppressed the growth of ovarian cancer cells, caused cell cycle blockage, and induced necrosis and apoptosis with more severe phenotypes observed in HeyA8 cells with wild-type p53 than in OVCAR-8 cells with mutant p53. P5091 also prompted autophagy, with more efficient p62 degradation in HeyA8. Conclusion: P5091 shows efficacy in suppressing ovarian cancers harbouring wild-type and mutant p53. Its effects seemed to be enhanced by wild-type p53. The potency of this USP7 inhibitor also correlated with autophagy to some extent. Therefore, the pharmacological targeting of USP7 may serve as a potential therapeutic strategy and warrants further investigation.

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Luo, Gang, Miao Wang, Xinchao Wu, Dan Tao, Xinyuan Xiao, Liang Wang, Fan Min, Fuqing Zeng, and Guosong Jiang. "Long Non-Coding RNA MEG3 Inhibits Cell Proliferation and Induces Apoptosis in Prostate Cancer." Cellular Physiology and Biochemistry 37, no. 6 (2015): 2209–20. http://dx.doi.org/10.1159/000438577.

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Background/Aims: Long non-coding RNAs (lncRNAs) play important roles in diverse biological processes, such as cell growth, apoptosis and migration. Although downregulation of lncRNA maternally expressed gene 3 (MEG3) has been identified in several cancers, little is known about its role in prostate cancer progression. The aim of this study was to detect MEG3 expression in clinical prostate cancer tissues, investigate its biological functions in the development of prostate cancer and the underlying mechanism. Methods: MEG3 expression levels were detected by qRT-PCR in both tumor tissues and adjacent non-tumor tissues from 21 prostate cancer patients. The effects of MEG3 on PC3 and DU145 cells were assessed by MTT assay, colony formation assay, western blot and flow cytometry. Transfected PC3 cells were transplanted into nude mice, and the tumor growth curves were determined. Results: MEG3 decreased significantly in prostate cancer tissues relative to adjacent normal tissues. MEG3 inhibited intrinsic cell survival pathway in vitro and in vivo by reducing the protein expression of Bcl-2, enhancing Bax and activating caspase 3. We further demonstrated that MEG3 inhibited the expression of cell cycle regulatory protein Cyclin D1 and induced cell cycle arrest in G0/G1 phase. Conclusions: Our study presents an important role of MEG3 in the molecular etiology of prostate cancer and implicates the potential application of MEG3 in prostate cancer therapy.

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Swietach, Pawel, Richard D. Vaughan-Jones, Adrian L. Harris, and Alzbeta Hulikova. "The chemistry, physiology and pathology of pH in cancer." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1638 (March 19, 2014): 20130099. http://dx.doi.org/10.1098/rstb.2013.0099.

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Cell survival is conditional on the maintenance of a favourable acid–base balance (pH). Owing to intensive respiratory CO 2 and lactic acid production, cancer cells are exposed continuously to large acid–base fluxes, which would disturb pH if uncorrected. The large cellular reservoir of H + -binding sites can buffer pH changes but, on its own, is inadequate to regulate intracellular pH. To stabilize intracellular pH at a favourable level, cells control trans-membrane traffic of H + -ions (or their chemical equivalents, e.g. ) using specialized transporter proteins sensitive to pH. In poorly perfused tumours, additional diffusion-reaction mechanisms, involving carbonic anhydrase (CA) enzymes, fine-tune control extracellular pH. The ability of H + -ions to change the ionization state of proteins underlies the exquisite pH sensitivity of cellular behaviour, including key processes in cancer formation and metastasis (proliferation, cell cycle, transformation, migration). Elevated metabolism, weakened cell-to-capillary diffusive coupling, and adaptations involving H + /H + -equivalent transporters and extracellular-facing CAs give cancer cells the means to manipulate micro-environmental acidity, a cancer hallmark. Through genetic instability, the cellular apparatus for regulating and sensing pH is able to adapt to extracellular acidity, driving disease progression. The therapeutic potential of disturbing this sequence by targeting H + /H + -equivalent transporters, buffering or CAs is being investigated, using monoclonal antibodies and small-molecule inhibitors.

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Liu, Xuejiao, Yulong Chong, Huize Liu, Yan Han, and Mingshan Niu. "CRM1 inhibitor S109 suppresses cell proliferation and induces cell cycle arrest in renal cancer cells." Korean Journal of Physiology & Pharmacology 20, no. 2 (2016): 161. http://dx.doi.org/10.4196/kjpp.2016.20.2.161.

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Short, Ben. "Determining the dynamics of cancer cell secretion." Journal of General Physiology 151, no. 12 (November 12, 2019): 1333. http://dx.doi.org/10.1085/jgp.201912518.

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Chen, Lujun, Wensi Zhai, Xiao Zheng, Quanqin Xie, Qi Zhou, Min Tao, Yibei Zhu, Changping Wu, and Jingting Jiang. "Decreased IFIT2 Expression Promotes Gastric Cancer Progression and Predicts Poor Prognosis of the Patients." Cellular Physiology and Biochemistry 45, no. 1 (December 22, 2017): 15–25. http://dx.doi.org/10.1159/000486219.

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Background/Aims: The status of interferon (IFN) signaling pathway has been shown to be closely associated with the response of immune checkpoint blockade therapy against advanced human cancers. IFN-induced protein with tetratricopeptide repeats 2 (IFIT2), also known as IFN-stimulated gene 54 (ISG54), is one of the most highly responsive ISGs, which can inhibit the proliferation and migration of cancer cells, and regulate viral replication, resulting in anti-cancer and anti-viral effects. In the present study, we aimed to investigate the role of IFIT2 in human gastric cancer. Methods: Immunohistochemistry assay was used to investigate the correlation between the IFIT2 expression in cancer tissues and clinical parameters of gastric cancer patients. Knockdown of IFIT2 was performed using RNAi to assess the role of IFIT2 in the regulation of biological behaviors in human gastric cancer cell lines. Results: IFIT2 expression in gastric cancer tissues was significantly associated with tumor stage and postoperative prognoses of the patients. Moreover, decreased IFIT2 expression in human gastric cancer cell lines SGC-7901 and AGS significantly increased the cell viability, cell migration and the ratios of cells in S phase. Conclusion: Our present study demonstrated that the decreased IFIT2 expression could promote the gastric cancer progression and predict poor therapeutic outcomes of the patients.

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Zhi, Yi, Jinhong Pan, Wenhao Shen, Peng He, Ji Zheng, Xiaozhou Zhou, Gensheng Lu, Zhiwen Chen, and Zhansong Zhou. "Ginkgolide B Inhibits Human Bladder Cancer Cell Migration and Invasion Through MicroRNA-223-3p." Cellular Physiology and Biochemistry 39, no. 5 (2016): 1787–94. http://dx.doi.org/10.1159/000447878.

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Background/Aims: Ginkgolide B (GB) is currently used as an anticancer drug for treatment of some malignant cancers. However, whether it may have therapeutic effects on bladder cancer remains unknown. Here, we studied the effects of GB on bladder cancer cells. Methods: Bladder cells were treated with different doses of GB, and the effects on ZEB1 and microRNA-223-3p (miR-223-3p) were analyzed by RT-qPCR and/or Western blot. Prediction of a regulatory relationship between miR-93 and 3'-UTR of Beclin-1 mRNA was performed by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay. Results: We found that GB dose-dependently decreased ZEB1 protein, but not mRNA, in bladder cancer cells, resulting in suppression of cell invasion. Moreover, in bladder cancer cells, GB dose-dependently decreased the levels of miR-223-3p, which suppressed the protein translation of ZEB1 through binding to 3'-UTR of ZEB1 mRNA. Overexpression of miR-223-3p decreased ZEB1 protein, while depletion of miR-223-3p increased ZEB1 protein in bladder cancer cells. Conclusion: GB inhibits bladder cancer cell invasiveness through suppressing ZEB1 protein translation via upregulating miR-223-3p.

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Sun, Pengcheng, Xinhai Sun, Weiming Zhao, Minghua Ren, Cheng Zhang, Ziqi Wang, and Wanhai Xu. "Lemur Tyrosine Kinase-3 Suppresses Growth of Prostate Cancer Via the AKT and MAPK Signaling Pathways." Cellular Physiology and Biochemistry 42, no. 6 (2017): 2582–92. http://dx.doi.org/10.1159/000480220.

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Background/Aims: Lemur tyrosine kinase (LMTK)-3 is a member of the receptor tyrosine kinase (RTK) family. Abnormal expression of LMTK-3 exists in various types of cancers, especially in endocrine-resistant breast cancers; however, the precise level of expression and the biological function in prostate cancer are poorly understood. Methods: In the present study, we determined the expression of LMTK-3 in prostate cancer using immunohistochemistry and Western blotting. We infected PC3 and LNCaP cells with lentivirus-LMTK-3 and observed the biologic characteristics of the PC3 and LNCaP cells in vitro with TUNEL, and migration and invasion assays, respectively. We also established a transplant tumor model of human prostate cancer with infected cells in 15 BALB/c-nu/nu nude mice. Results: LMTK-3 was expressed in prostate epithelial cells. There was a significant decline in the level of LMTK-3 expression in prostate cancers compared to normal tissues. LMTK-3 inhibited PC3 and LNCaP cell growth, migration, and invasion, and induced cell apoptosis in vitro. We also observed that LMTK-3 induced PC3 cell apoptosis in vivo. Further study showed that LMTK-3 inhibited phosphorylation of AKT and ERK, and promoted phosphorylation and activation of p38 kinase and Jun kinase (JNK). Conclusion: Recombinant lentivirus with enhanced expression of LMTK-3 inhibited prostate cancer cell growth and induced apoptosis in vitro and in vivo. AKT and MAPK signaling pathways may contribute to the process.

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Yang, Chen, Qing Ou Yang, Qing-Jie Kong, Wen Yuan, and Yue-Ping Ou Yang. "Parthenolide Induces Reactive Oxygen Species-Mediated Autophagic Cell Death in Human Osteosarcoma Cells." Cellular Physiology and Biochemistry 40, no. 1-2 (2016): 146–54. http://dx.doi.org/10.1159/000452532.

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Background and Aim: Osteosarcoma is a devastating tumor of bone, primarily affecting adolescents. Parthenolide, a naturally occurring small molecule that interferes with NF-κB signaling, has recently attracted considerable attention because of its pharmacological action involving anti-cancer effects. However, the mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. Methods: In this study, the effects of parthenolide were evaluated and characterized in human osteosarcoma cancer cell. Cell viability was assessed by CCK-8. Apoptosis was assessed by Annexin V-FITC/PI Flow cytometry assay. Relative quantitative real-time PCR and western blot were used to determine the expressions of genes and proteins. Results: Our results suggest that parthenolide did not cause caspase-dependent cell death in osteosarcoma cancer cells, as indicated by the absence of significant early apoptosis as well as caspase-3 cleavage. Instead, parthenolide increased the autophagy and mitophagy, as characterized by increased PINK1 and Parkin translocation to mitochondria and enhanced autophagy proteins. The induction of autophagy by parthenolide was associated with the increase of reactive oxygen species (ROS). ROS antioxidants N-acetylcysteine (NAC) attenuated parthenolide-induced autophagy activity. Conclusions: Our findings unveil a novel mechanism of drug action by parthenolide in osteosarcoma cancer cells and suggest a potential value of treating osteosarcoma cancer through a caspase-independent autophagic cell death by ROS activation.

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Tanigawa, Tetsuya, Rama Pai, Tetsuo Arakawa, and Andrzej S. Tarnawski. "Rebamipide Inhibits Gastric Cancer Cell Growth." Digestive Diseases and Sciences 52, no. 1 (December 14, 2006): 240–47. http://dx.doi.org/10.1007/s10620-006-9226-x.

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Liu, Pei-Feng, Chien-Jen Hsu, Wei-Lun Tsai, Jin-Shiung Cheng, Jih-Jung Chen, I.-Fei Huang, Ho-Hsing Tseng, Hsueh-Wei Chang, and Chih-Wen Shu. "Ablation of ATG4B Suppressed Autophagy and Activated AMPK for Cell Cycle Arrest in Cancer Cells." Cellular Physiology and Biochemistry 44, no. 2 (2017): 728–40. http://dx.doi.org/10.1159/000485286.

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Background/Aims: ATG4B is a cysteine protease required for autophagy, which is a cellular catabolic pathway involved in energy balance. ATG4B expression is elevated during tumor growth in certain types of cancer, suggesting that ATG4B is an attractive target for cancer therapy. However, little is known about the mechanisms through which ATG4B deprivation suppresses the growth of cancer cells. Methods: Cancer cells were transfected with either siRNA against ATG4B or an expression vector encoding wild-type ATG4BWT or encoding catalytic mutant ATG4BC74A to determine cell cycle progression by propidium iodide staining or by BrdU incorporation assay using flow cytometry. The GFP-MAP1LC3-II puncta and protein levels in the cells were determined by immunofluorescence and immunoblotting, respectively. Results: Knockdown of ATG4B blocked cell proliferation, particularly at the G1-S phase transition, in various cancer cells. Moreover, knockdown of ATG4B or overexpression of the ATG4BC74A catalytic mutant reduced both autophagic flux and ATP levels and increased AMP-activated protein kinase (AMPK) phosphorylation in the cancer cells. Nevertheless, knockdown of ATG4B had only a minor effect on AMPK activation and G1 phase arrest in liver kinase B1 (LKB1)-deficient or AMPK-inhibited cancer cells. Conclusion: These results imply that targeting ATG4B might inhibit autophagy and trigger the LKB1-AMPK energy-sensing pathway, resulting in tumor growth suppression.

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Deng, Youlin, Zhongliang Wang, Fugui Zhang, Min Qiao, Zhengjian Yan, Qiang Wei, Jing Wang, et al. "A Blockade of IGF Signaling Sensitizes Human Ovarian Cancer Cells to the Anthelmintic Niclosamide-Induced Anti-Proliferative and Anticancer Activities." Cellular Physiology and Biochemistry 39, no. 3 (2016): 871–88. http://dx.doi.org/10.1159/000447797.

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Background/Aims: Ovarian cancer is the most lethal gynecologic malignancy, and there is an unmet clinical need to develop new therapies. Although showing promising anticancer activity, Niclosamide may not be used as a monotherapy. We seek to investigate whether inhibiting IGF signaling potentiates Niclosamide's anticancer efficacy in human ovarian cancer cells. Methods: Cell proliferation and migration are assessed. Cell cycle progression and apoptosis are analyzed by flow cytometry. Inhibition of IGF signaling is accomplished by adenovirus-mediated expression of siRNAs targeting IGF-1R. Cancer-associated pathways are assessed using pathway-specific reporters. Subcutaneous xenograft model is used to determine anticancer activity. Results: We find that Niclosamide is highly effective on inhibiting cell proliferation, cell migration, and cell cycle progression, and inducing apoptosis in human ovarian cancer cells, possibly by targeting multiple signaling pathways involved in ELK1/SRF, AP-1, MYC/MAX and NFkB. Silencing IGF-1R exert a similar but weaker effect than that of Niclosamide's. However, silencing IGF-1R significantly sensitizes ovarian cancer cells to Niclosamide-induced anti-proliferative and anticancer activities both in vitro and in vivo. Conclusion: Niclosamide as a repurposed anticancer agent may be more efficacious when combined with agents that target other signaling pathways such as IGF signaling in the treatment of human cancers including ovarian cancer.

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McDonald, P. C., A. B. Fielding, and S. Dedhar. "Integrin-linked kinase - essential roles in physiology and cancer biology." Journal of Cell Science 121, no. 19 (October 1, 2008): 3121–32. http://dx.doi.org/10.1242/jcs.017996.

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Li, Li, Yingying Geng, Ru Feng, Qinqin Zhu, Bei Miao, Jiang Cao, and Sujuan Fei. "The Human RNA Surveillance Factor UPF1 Modulates Gastric Cancer Progression by Targeting Long Non-Coding RNA MALAT1." Cellular Physiology and Biochemistry 42, no. 6 (2017): 2194–206. http://dx.doi.org/10.1159/000479994.

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Background/Aims: The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is overexpressed in numerous cancers. However, whether MALAT1 is regulated and the related mechanisms in gastric cancer remain unclear. Methods: Immunohistochemistry and qRT-PCR analyses were used to detect the expression levels of UPF1 and MALAT1 in gastric cancer and adjacent normal tissues. MTT, cell cycle, apoptosis and transwell assays were performed to examine the effects of UPF1 on cell cycle progression, cell proliferation, apoptosis, migration and invasion. Additionally, sodium bisulfate sequencing was used to test the promoter hypermethylation on UPF1 in gastric tumor tissues. Finally, RNA immunoprecipitation and luciferase reporter analyses demonstrated that UPF1 directly bound with MALAT1. Results: The expression of UPF1 was significantly downregulated in gastric cancer and negatively correlated with MALAT1 expression. Patients with lower expression of UPF1 had poorer prognosis than those with higher expression. Overexpression of UPF1 inhibited cell proliferation, cell cycle progression, cell migration and invasion, and promoted cell apoptosis in gastric cancer cells. Moreover, the UPF1-mediated inhibition of gastric cancer progression was reversed by overexpression of MALAT1. A profound downregulation of UPF1 in gastric tumor tissues was due to promoter hypermethylation. Overexpression of UPF1 increased nonsense-mediated mRNA decay (NMD) efficiency and thus led to downregulation of MALAT1. Conclusion: Our results demonstrate that UPF1 is a potential modulator of MALAT1 and that UPF1/MALAT1 pathway could be a therapeutic target for gastric cancer.

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Gao, Yanping, Bing Feng, Siqi Han, Lu Lu, Yitian Chen, Xiaoyuan Chu, Rui Wang, and Longbang Chen. "MicroRNA-129 in Human Cancers: from Tumorigenesis to Clinical Treatment." Cellular Physiology and Biochemistry 39, no. 6 (2016): 2186–202. http://dx.doi.org/10.1159/000447913.

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Emerging evidence has shown that microRNAs (miRNAs) play essential roles in regulating human cancers development and progression. However, the underlying mechanisms remain to be further explored. MiRNAs are a class of endogenous, non-coding, 18-24 nucleotide length single-strand RNAs that moderate gene expression primarily at post-transcriptional level. There is a growing body of literature that recognizes the importance of microRNA (miR)-129 during the development of cancers. Aberrant expression of miR-129 has been detected in various types of human cancers and the validated target genes are involved in cancer-related biological processes such as DNA methylation, cell proliferation, apoptosis, cell cycle, and metastasis. In this review, we summarized the roles of miR-129 family members and their target genes in tumorigenesis and clinical treatment of human cancers, highlighting the potential roles of miR-129 as biomarkers for cancer diagnosis and prognosis, and promising tools for cancer treatment.

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You, Changxuan, Yu Yang та Beili Gao. "Imperatorin Targets MCL-1 to Sensitize CD133+ Lung Cancer Cells to γδ-T Cell-Mediated Cytotoxicity". Cellular Physiology and Biochemistry 49, № 1 (2018): 235–44. http://dx.doi.org/10.1159/000492874.

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Background/Aims: CD133+ cancer cells display low sensitivity to anti-cancer treatment; thus, combination treatment with adjuvant drugs is required to improve the efficiency of cancer therapy. The aim of this study was to explore the effect of imperatorin, a linear furanocoumarin compound, on γδ T cell-mediated cytotoxicity against CD133+ lung cancer cells. Methods: CD133+ and CD133- subgroups from A549 and PC9 lung cancer cells were sorted by using flow cytometry. The cytotoxicity of γδ T cells against cancer cells was evaluated by measuring lactate dehydrogenase release. The concentration of tumor necrosis factor-related apoptosis-inducing ligand in the co-culture system was determined by using an enzyme-linked immunosorbent assay. Mitochondrial membrane potential, expression of death receptor 4 (DR4) and DR5 on the cell surface, and rate of apoptosis were measured by flow cytometry. Cytochrome c release and cellular protein expression were detected by western blot analysis. Results: Compared with CD133- cells, CD133+ cells were resistant to γδ T cell-mediated cytotoxicity. However, imperatorin significantly increased the sensitivity of CD133+ lung cancer cells to γδ T cell treatment in vitro and in vivo. Mechanically, we found that myeloid cell leukemia 1 (MCL-1), an important anti-apoptotic protein belonging to the Bcl-2 family, was overexpressed in CD133+ A549 and PC9 cells compared to their corresponding CD133- cells. Co-treatment with imperatorin and γδ T cells suppressed the expression of MCL-1, and thus promoted the mitochondrial apoptosis mediated by γδ T cells in CD133+ A549 and PC9 lung cancer cells. Conclusion: Up-regulated MCL-1 in CD133+ lung cancer cells is responsible for their resistance to γδ T cells. Furthermore, the combination of γδ T cells with imperatorin sensitized CD133+ lung cancer cells to γδ T cell-mediated cytotoxicity by targeting MCL-1.

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Hiraoka, Kenji, Hiroaki Miyazaki, Naomi Niisato, Yoshinobu Iwasaki, Akihiro Kawauchi, Tsuneharu Miki, and Yoshinori Marunaka. "Chloride Ion Modulates Cell Proliferation of Human Androgen-independent Prostatic Cancer Cell." Cellular Physiology and Biochemistry 25, no. 4-5 (2010): 379–88. http://dx.doi.org/10.1159/000303042.

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