Journal articles on the topic 'MiR-194'
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1
Tang, Hao, Ping Gong, Ling Tao, and Yurong Hua. "miR-194 Inhibits Ovarian Cancer Cell Proliferation and Reduces Cisplatin Resistance by Targeting Yes-Associated Protein." Journal of Biomaterials and Tissue Engineering 10, no. 8 (August 1, 2020): 1170–75. http://dx.doi.org/10.1166/jbt.2020.2379.
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Elevated expression of Yes-associated protein (YAP1) is associated with ovarian cancer. Bioinformatics analysis showed a relationship between miR-194 and YAP1. Our study intends to assess whether miR-194 regulates YAP1 expression and affects the proliferation of ovarian cancer cells and CDDP resistance. CDDP-resistant cell line A2780/CDDP was established and the expression of miR-194 and YAP1 in parental A2780 cells and normal ovarian epithelial IOSE80 cells were compared. A2780/CDDP cells were separated into miR-NC group and miR-194 mimic group followed by analysis of miR-194 and YAP1 expression, and cell apoptosis and proliferation by flow cytometry. There was a targeted relationship between miR-194 and YAP1 mRNA. A2780/CDDP cells had the lowest miR-194 expression followed by A2780 cells and IOSE80 cells. In addition, YAP1 level was highest in A2780/CDDP cells followed by A2780 cells and IOSE80 cells. Compared with miR-NC group, miR-194 expression was significantly increased in miR-194 mimic transfection group and YAP1 protein expression was significantly decreased, with increased cell apoptosis and reduced cell proliferation ability. Decreased miR-194 expression and increased YAP1 expression are related to ovarian cancer CDDP resistance. Increased miR-194 can down-regulate YAP1, inhibit ovarian cancer cell proliferation, promote cell apoptosis, and reduce CDDP resistance.
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Wu, Lei, Si Cheng, Yong Meng, and Yahui Huang. "miR-194 Regulates Cisplatin Resistance in Colorectal Cancer Cells Through Targeting Yes-Associated Protein." Journal of Biomaterials and Tissue Engineering 10, no. 2 (February 1, 2020): 157–62. http://dx.doi.org/10.1166/jbt.2020.2239.
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Elevated Yes-associated protein (YAP1) expression is associated with colorectal cancer. Bioinfor-matics analysis showed a targeting relationship between miR-194 and YAP13′-UTR. Our study assessed miR-194’s role in proliferation, apoptosis, and CDDP resistance of colorectal cancer cells. The CDDP-resistant cell line SW480/CDDP was established and miR-194 and YAP1 level in parental SW480 cells and normal intestinal epithelial HCoEpiC cells was measured. SW480/CDDP cells were separated into control group, miR-NC group and miR-194 mimic group followed by analysis of miR-194 and YAP1 level, cell apoptosis and proliferation by flow cytometry. There was a targeted regulatory relationship between miR-194 and YAP1 mRNA. miR-194 was significantly upregulated in SW480/CDDP cells compared to SW480 cells and downregulated in SW480 cells compared to HCoEpiC cells. Whereas, opposite YAP1 expression profiles were found in SW480/CDDP, SW480 and HCoEpiC cells. miR-194 mimic significantly upregulated miR-194 in the SW480/CDDP cells, with decreased YAP1 expression, increased cell apoptosis, decreased cell proliferation and reduced IC50. Decreased miR-194 and increased YAP1 expression involve in CDDP resistance of colorectal cancer. Increase of miR-194 expression can inhibit colorectal cancer cell proliferation, promote apoptosis and reduce CDDP resistance by down-regulating YAP1 expression.
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Lin, Dao-Hong, Peng Yue, Chengbiao Zhang, and Wen-Hui Wang. "MicroRNA-194 (miR-194) regulates ROMK channel activity by targeting intersectin 1." American Journal of Physiology-Renal Physiology 306, no. 1 (January 1, 2014): F53—F60. http://dx.doi.org/10.1152/ajprenal.00349.2013.
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The aim of the study is to explore the role of miR-194 in mediating the effect of high-K (HK) intake on ROMK channel. Northern blot analysis showed that miR-194 was expressed in kidney and that HK intake increased while low-K intake decreased the expression of miR-194. Real-time PCR analysis further demonstrated that HK intake increased the miR-194 expression in the cortical collecting duct. HK intake decreased the expression of intersectin 1 (ITSN1) which enhanced With-No-Lysine Kinase (WNK)-induced endocytosis of ROMK. Expression of miR-194 mimic decreased luciferase reporter gene activity in HEK293 T cells transfected with ITSN-1–3′UTR containing the complementary seed sequence for miR-194. In contrast, transfection of miR-194 inhibitor increased the luciferase activity. This effect was absent in the cells transfected with mutated 3′UTR of ITSN1 in which the complimentary seed sequence was deleted. Moreover, the inhibition of miR-194 expression increased the protein level of endogenous ITSN1 in HEK293T cells. Expression of miR-194 mimic also decreased the translation of exogenous ITSN1 in the cells transfected with the ITSN1 containing 3′UTR but not with 3′UTR-free ITSN1. Expression of pre-miR-194 increased K currents and ROMK expression in the plasma membrane in ROMK-transfected cells. Coexpression of ITSN1 reversed the stimulatory effect of miR-194 on ROMK channels. This effect was reversed by coexpression of ITSN1. We conclude that miR-194 regulates ROMK channel activity by modulating ITSN1 expression thereby enhancing ITSN1/WNK-dependent endocytosis. It is possible that miR-194 is involved in mediating the effect of a HK intake on ROMK channel activity.
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Miao, Jinglei, Weiguo Wang, Song Wu, Xiaofang Zang, Yuezhan Li, Jianlong Wang, Ruisen Zhan, et al. "miR-194 Suppresses Proliferation and Migration and Promotes Apoptosis of Osteosarcoma Cells by Targeting CDH2." Cellular Physiology and Biochemistry 45, no. 5 (2018): 1966–74. http://dx.doi.org/10.1159/000487973.
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Background/Aims: Studies have shown that miR-194 functions as a tumour suppressor and is associated with tumour growth and metastasis. This study intends to uncover the mechanism of tumour suppression by miR-194. The expression of miR-194 in osteosarcoma cell lines and tissues were monitored by real-time PCR. Methods: The proliferation ability was examined by MTT assay. Migration and apoptosis of cells were monitored by migration assay and flow cytometry, respectively. The regulation of miR-194 on CDH2 was determined by luciferase assays and western blot assays. Results: The results showed that miR-194 was significantly reduced in osteosarcoma compared with that in normal bone tissue. Overexpression of miR-194 significantly attenuated the proliferation and migration and induced the apoptosis of osteosarcoma cells. Furthermore, we demonstrated that miR-194 has inhibited the malignant behaviour of osteosarcoma by downregulating CDH2 expression. Conclusions: These findings suggested that miR-194 may act as a tumour suppressor in osteosarcoma. miR-194/CDH2 may be a novel therapeutic target in the treatment of osteosarcoma.
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Cui, Guanghui, Donglei Liu, Weihao Li, Yuhang Li, Youguang Liang, Wensong Shi, and Song Zhao. "Original Research: miR-194 inhibits proliferation and invasion and promotes apoptosis by targeting KDM5B in esophageal squamous cell carcinoma cells." Experimental Biology and Medicine 242, no. 1 (August 10, 2016): 45–52. http://dx.doi.org/10.1177/1535370216662712.
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Increasing evidence suggests that miR-194 is down-regulated in esophageal squamous cell carcinoma tumor tissue. However, the role and underlying mechanism of miR-194 in esophageal squamous cell carcinoma have not been well defined. We used DIANA, TargetScan and miRanda to perform target prediction analysis and found KDM5B is a potential target of miR-194. Based on these findings, we speculated that miR-194 might play a role in esophageal squamous cell carcinoma development and progression by regulation the expression of KDM5B. We detected the expression of miR-194 and KDM5B by quantitative real-time reverse transcription PCR (qRT-PCR) and Western blot assays, respectively, and found down-regulation of miR-194 and up-regulation of KDM5B existed in esophageal squamous cell carcinoma cell lines. By detecting proliferation, invasion and apoptosis of TE6 and TE14 cells transfected with miR-194 mimics or mimic control, miR-194 was found to inhibit proliferation and invasion and promote apoptosis of esophageal squamous cell carcinoma cells. miR-194 was further verified to regulate proliferation, apoptosis and invasion of esophageal squamous cell carcinoma cells by directly targeting KDM5B. Furthermore, animal studies were performed and showed that overexpression of miR-194 inhibited the growth of esophageal squamous cell carcinoma tumors in vivo. These results confirmed our speculation that miR-194 targets KDM5B to inhibit esophageal squamous cell carcinoma development and progression. These findings offer new clues for esophageal squamous cell carcinoma development and progression and novel potential therapeutic targets for esophageal squamous cell carcinoma.
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Jenkins, Robert H., John Martin, Aled O. Phillips, Timothy Bowen, and Donald J. Fraser. "Transforming growth factor β1 represses proximal tubular cell microRNA-192 expression through decreased hepatocyte nuclear factor DNA binding." Biochemical Journal 443, no. 2 (March 27, 2012): 407–16. http://dx.doi.org/10.1042/bj20111861.
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miR (microRNA)-192 plays key roles in renal pathological and physiological responses, by repressing targets including Zeb1, Zeb2 and Wnk1. In the present study, we have assessed the regulation of miR-192 expression. We found that TGF-β1 (transforming growth factor β1) down-regulates miR-192 and miR-194, co-transcribed in the shared precursor pri-miR (primary miR transcript)-192/194. Luciferase reporter analysis showed constitutive promoter activity within nucleotides +21 to −223. We identified HNF (hepatocyte nuclear factor) and p53 binding sites within this region that were required for constitutive promoter activity, which was decreased by TGF-β1 through an Alk5-dependent mechanism. TGF-β1 treatment decreased HNF binding to the miR-194-2/192 promoter, whereas knockdown of HNF-1 inhibited mature miR-192 and miR-194 expression. miR-192, miR-194 and HNF expression were restricted to a defined subset of human tissues including kidney, small intestine, colon and liver. Our results from the present study identify co-ordinated regulation of miR-192 and miR-194, with binding of HNF and p53 transcription factors necessary for activation of transcription, and TGF-β1-mediated repression through decreased HNF binding to its cognate promoter element.
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Xu, Zhishan, Bingyu Guo, Peng Chang, Qiang Hui, Wei Li, and Kai Tao. "The Differential Expression of miRNAs and a Preliminary Study on the Mechanism of miR-194-3p in Keloids." BioMed Research International 2019 (March 7, 2019): 1–10. http://dx.doi.org/10.1155/2019/8214923.
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The aim of this study was to detect abnormally expressed microRNA (miRNA) in keloids and to study their functions. The differential expression of miRNAs in keloids and normal tissue was detected by gene microarray. MiRNA expression was verified by real-time PCR. A luciferase reporter gene assay, western blot, and real-time PCR were used to detect the effect of miR-194-3p on RUNX2. An MTT assay and a transwell assay were used to detect the effect of miR-194-3p in both primary cultured fibroblasts and HKF cells. Related proteins were analysed by western blot and real-time PCR. The expression of miR-194-3p was lower in keloids, and MiR-194-3p was shown to target RUNX2 directly. MiR-194-3p inhibited the proliferation and migration of fibroblasts through the inhibition of CDK4 and MMP2. MiR-194-3p and RUNX2 may become new targets for the prevention and treatment of keloids.
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Yen, Yu-Ting, Jou-Chun Yang, Jiun-Bo Chang, and Shih-Chang Tsai. "Down-Regulation of miR-194-5p for Predicting Metastasis in Breast Cancer Cells." International Journal of Molecular Sciences 23, no. 1 (December 28, 2021): 325. http://dx.doi.org/10.3390/ijms23010325.
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MicroRNAs (miRNAs), as key negative regulators of gene expression, are closely related to tumor occurrence and progression. miR-194-5p (miR-194-1) has been shown to play a regulatory role in various cancers however, its biological function and mechanism of action in breast cancer have not yet been well explored. In this study, we use the UALCAN and LinkedOmics databases to analyze transcription expression in The Cancer Genome Atlas Breast Invasive Carcinoma (TCGA-BRCA). The epithelial-mesenchymal transition status of breast cancer cells was evaluated by wound-healing assay, trans-well assays, and gelatin zymography, while protein expression was assessed by Western blotting. miR-194-5p expression was found to be up-regulated in breast cancer clinical specimens but down-regulated in the triple-negative breast cancer (TNBC) cell line MDA-MB-231 and breast cancer clinical specimens in The Cancer Genome Atlas (TCGA). miR-194-5p significantly inhibited the expression of the epithelial marker ZO-1 and increased the expression of mesenchymal markers, including ZEB-1 and vimentin, in MDA-MB-231 cells. miR-194-5p significantly reduced the gelatin-degrading activity of matrix metalloproteinase-2 (MMP-2) and MMP-9 in zymography assays. In MDA-MB-231 cells and TCGA patient samples, ZEB-1 expression was significantly inversely correlated with miR-194-5p expression. High levels of miR-194-5p were associated with good overall survival. miR-194-5p regulates epithelial–mesenchymal transition (EMT) in TNBC. Our findings suggest that miR-194-5p functions as a tumor biomarker in breast cancer, providing new insights for the study of breast cancer development and metastasis.
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Niu, Tong, Liuzhong Jin, Shizhen Niu, Cunqi Gong, and Hui Wang. "Lycium Barbarum Polysaccharides Alleviates Oxidative Damage Induced by H2O2 Through Down-Regulating MicroRNA-194 in PC-12 and SH-SY5Y Cells." Cellular Physiology and Biochemistry 50, no. 2 (2018): 460–72. http://dx.doi.org/10.1159/000494159.
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Background/Aims: Currently, scientists attempt to improve outcome of spinal cord injury (SCI) via reducing secondary injury during SCI. Oxidative stress is critical for pathophysiology of secondary damage, thus we mainly focused on the anti-oxidant effects of Lycium barbarum polysaccharides (LBPs) on PC-12 and SH-SY5Y cells as well as the underlying mechanisms. Methods: Oxidative stress was induced by H2O2 stimulation. Effects of LBPs on cell viability, apoptosis, and expression of proteins associated with apoptosis and autophagy in H2O2-induced cells were assessed by CCK-8 assay, flow cytometry assay and Western blot analysis, respectively. Then, expression of miR-194 was determined by qRT-PCR. Expression of miR-194 was dysregulated, and whether LBPs affected H2O2-treated cells through modulating miR-194 was verified. The expression of key kinases in the PI3K/AKT pathway and the intracellular levels of ROS and NO were testified by Western blot analysis and flow cytometry with fluorescent probes. Results: H2O2-induced decrease of cell viability and increases of apoptosis and autophagy in PC-12 cells were mitigated by LBPs treatment. Next, we found that miR-194 expression was both down-regulated by LBPs treatment in PC-12 and SH-SY5Y cells. More experiments consolidated that influence of LBPs on H2O2-treated cells was reversed by miR-194 overexpression while was augmented by miR-194 inhibition. LBPs elevated the phosphorylated levels of PI3K and AKT and reduced levels of ROS and NO through miR-194. Conclusion: LBPs alleviated H2O2-induced decrease of cell viability, and increase of apoptosis and autophagy through down-regulating miR-194. Moreover, LBPs activated the PI3K/AKT pathway and reduced oxidative stress through miR-194.
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Li, Chang-feng, Yong-chao Li, Yun Wang, and Li-bo Sun. "The Effect of LncRNA H19/miR-194-5p Axis on the Epithelial-Mesenchymal Transition of Colorectal Adenocarcinoma." Cellular Physiology and Biochemistry 50, no. 1 (2018): 196–213. http://dx.doi.org/10.1159/000493968.
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Background/Aims: Since the combined actions of lncRNAs and miRNAs have been considered to be involved in the occurrence and development of various neoplasms, the main purpose of this study was to discover whether and how lncRNA H19 and miR-194 influenced the epithelial-mesenchymal transition (EMT) process of colorectal adenocarcinoma (CRA). Methods: Totally 214 pairs of CRA and adjacent normal tissues were collected, and 5 human CRA cell lines (i.e. HCT116, HT-29, RKO SW280 and Lovo) were purchased. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) was adopted to quantify the H19 and miR-194-5p expressions in cells and tissues. The expressions of FoxM1, E-cadherin, vimentin, N-cadherin were determined using western blot. On the side, si-H19, si-NC, miR-194-5p mimic, miR-194-5p inhibitor and negative control (NC) were transfected into CRA cell lines. Meanwhile, the invasive, migratory and proliferative conditions of the cells were assessed through transwell, wound healing and colony-forming experiments, with final verification of the relationship between H19 and miR-194-5p employing dual-luciferase reporter gene assay. Results: Highly-expressed H19, lowly-expressed miR-194-5p, low-grade differentiation and lymph node metastasis appeared as the independent predictors of unfavorable prognosis in CRA patients’ (all P< 0.05). It indicated that FoxM1 expression displayed positive correlations with H19 expression, yet negative associations with miR-194-5p expression within CRA tissues (P< 0.05). In addition, transfection of H19-siRNA and miR-145-5p mimic triggered a conspicuous increase in E-cadherin expression, as well as an evidently down-regulation in vimentin and N-cadherin expressions within HT29 and RKO cells (P< 0.05). On the other hand, the invasive and migratory capacities of CRA cells were significantly hindered (P< 0.05). Moreover, the luciferase reporter gene assay confirmed that H19 modified miR-194-5p expression through directly targeting at it (P< 0.05). Ultimately, FoxM1 could reverse the role of miR-194-5p in inhibiting invasion, migration and EMT of CRA cells (P< 0.05). Conclusion: LncRNA H19/miR-194/FoxM1 axis could serve as a profound target for the diagnosis and treatment of CRA.
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Shao, Yun, Zhengxiang Yang, Weifeng Miao, Xiangrong Yu, Yiping Wu, and Yi Pu. "circ_0030018 promotes glioma proliferation and metastasis." Translational Neuroscience 12, no. 1 (January 1, 2021): 260–72. http://dx.doi.org/10.1515/tnsci-2020-0175.
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Abstract Background Circular RNA (circRNA) plays an essential role in tumor progression, including glioma. circ_0030018 is a newly discovered circRNA that is highly expressed in glioma. However, its role and mechanism in glioma need to be further elucidated. Methods The expression of circ_0030018, microRNA (miR)-194-5p, and tripartite motif containing 44 (TRIM44) was examined using quantitative real-time PCR. Cell proliferation, migration, invasion, and apoptosis were determined using MTT assay, colony formation assay, transwell assay, and flow cytometry. Moreover, dual-luciferase reporter assay and RNA pull-down assay were used to verify the interactions among circ_0030018, miR-194-5p, and TRIM44. The protein expression of TRIM44 was assessed by western blot analysis. Animal experiments were conducted to explore the role of circ_0030018 in glioma tumor growth in vivo. Results circ_0030018 was overexpressed in glioma tissues and cells, and its silencing could inhibit glioma cell proliferation, migration, invasion, and accelerate apoptosis. miR-194-5p could be sponged by circ_0030018, and its overexpression could hinder the progression of glioma cells. Further experiments revealed that miR-194-5p inhibitor reversed the negative regulation of circ_0030018 knockdown on glioma cell progression. In addition, TRIM44 was a target of miR-194-5p, and its downregulation could repress glioma cell progression. Overexpressed TRIM44 reversed the inhibition effect of miR-194-5p on glioma cell progression. Animal experiments suggested that circ_0030018 knockdown could reduce glioma tumor growth through regulating miR-194-5p and TRIM44. Conclusion Our 8data showed that circ_0030018 enhanced glioma progression by sponging miR-194-5p to regulate TRIM44, indicating that circ_0030018 might be a potential treatment target for glioma.
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Xie, Fei, Lei Yang, Lili Han, and Bin Yue. "MicroRNA-194 Regulates Lipopolysaccharide-Induced Cell Viability by Inactivation of Nuclear Factor-κ B Pathway." Cellular Physiology and Biochemistry 43, no. 6 (2017): 2470–78. http://dx.doi.org/10.1159/000484453.
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The present study explored the functional role of microRNA (miR)-194 in lipopolysaccharide (LPS) induced lung cell injury, along with the underlying mechanisms and to reveal the potential role in infantile pneumonia. Human fibroblasts WI38 cells were transfected with miR-194 mimic or miR-194 inhibitor, and the transfection efficiency was confirmed by quantitative real-time polymerase chain reaction (qRT-PCR). Thereafter, the cells were treated with or without LPS, and then cell viability, cell apoptosis and mRNA and protein expressions of key proteins of nuclear factor kappa B (NF-κB) pathway including inhibitor of NF-κB (IκB) α, p-65, and B-cell CLL/lymphoma (Bcl) 3 were analyzed. Results showed that overexpression and suppression of miR-194 was effective. Administration of LPS significantly decreased the cell viability and statistically promoted the percentages of apoptotic cells and increased the mRNA and protein expressions of p-65 and Bcl-3 but downregulated IκBα compared to the control group (P < 0.05 or P < 0.01). LPS in combination with miR-194 suppression further enhanced the effects of LPS on cell viability and cell apoptosis compared to the LPS group (P < 0.05). In contrast, LPS in combination with miR-194 overexpression observably reversed the effects of LPS on cell viability, cell apoptosis and mRNA and protein expressions of the key proteins (P < 0.05 or P < 0.01). In conclusion, miR-194 increases the LPS-induced the inhibition of cell viability and increasing of the cell apoptosis by inhibition of NF-κB pathway in WI38 cells. MiR-194 might be a potential targeted therapy for treatment of infantile pneumonia.
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Zhang, Sheng-Xiong, Wen Tian, Yuan-Liang Liu, Jia-Hui Ni, Dan Zhang, Hua-Feng Pan, Zi-Ming Zhao, et al. "Mechanism of N-Methyl-N-Nitroso-Urea-Induced Gastric Precancerous Lesions in Mice." Journal of Oncology 2022 (March 16, 2022): 1–9. http://dx.doi.org/10.1155/2022/3780854.
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Early diagnosis and treatment of gastric precancerous lesions (GPL) are key factors for reducing the incidence and morbidity of gastric cancer. The study is aimed at examining GPL in mice induced by N-methyl-N-nitroso-urea (MNU) and to illustrate the underlying mechanisms of tumorigenesis. In this study, we utilized an in vivo MNU-induced GPL mouse model, and histopathological changes of the gastric mucosa were observed by hematoxylin and eosin (H&E-stain) and alcian blue (AB-PAS-stain). The level of miR-194-5p in the gastric mucosa was determined by real-time polymerase chain reaction. We used transmission electron microscopy to observe the effects of MNU on gastric chief cells and parietal cells. We performed immunohistochemical detection of HIF-1α, vWF, Ki-67, and P53, while the changes in the protein expression of key genes in LKB1-AMPK and AKT-FoxO3 signaling pathways were detected by western blot analysis. We demonstrated that the miR-194-5p expression was upregulated under hypoxia in GPL gastric tissues, and that a high miR-194-5p expression level closely related with tumorigenesis. Mechanistically, miR-194-5p exerted the acceleration of activities related to metabolic reprogramming through LKB1-AMPK and AKT-FoxO3 pathways. Furthermore, similar to miR-194-5p, high expression levels of AMPK and AKT were also related to the metabolic reprogramming of GPL. Moreover, we revealed the correlation between the expression levels of miR-194-5p, p-AMPKα, p-AKT, and FoxO3a. These findings suggest that miR-194-5p/FoxO3 pathway is important for the reversal of metabolic reprogramming in GPL. Thus, exploring strategies to regulate the miR-194-5p/FoxO3a pathway may provide an efficient strategy for the prevention and treatment of GPL.
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Wang, Tingting, Yaling Cheng, Haibin Han, Jie Liu, Bo Tian, and Xiaocui Liu. "miR-194 Accelerates Apoptosis of Aβ1–42-Transduced Hippocampal Neurons by Inhibiting Nrn1 and Decreasing PI3K/Akt Signaling Pathway Activity." Genes 10, no. 4 (April 21, 2019): 313. http://dx.doi.org/10.3390/genes10040313.
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This article explores the mechanism of miR-194 on the proliferation and apoptosis of Aβ1–42-transduced hippocampal neurons. Aβ1–42-transduced hippocampal neuron model was established by inducing hippocampal neurons with Aβ1–42. MTT assay and flow cytometry were used to detect the viability and apoptosis of hippocampal neurons, respectively. qRT-PCR was used to detect changes in miR-194 and Nrn1 expression after Aβ1–42 induction. Aβ1–42-transduced hippocampal neurons were transfected with miR-194 mimics and/or Nrn1 overexpression vectors. Their viability and neurite length were detected by MTT assay and immunofluorescence, respectively. Western blot was used to detect protein expression. Aβ1–42 inhibited Aβ1–42-transduced hippocampal neuron activity and promoted their apoptosis in a dose-dependent manner. miR-194 was upregulated and Nrn1 was downregulated in Aβ1–42-transduced hippocampal neurons (p < 0.05). Compared with the model group, Aβ1–42-transduced hippocampal neurons of the miR-194 mimic group had much lower activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much higher Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Compared with the model group, Aβ1–42-transduced hippocampal neurons of the LV-Nrn1 group had much higher activity, average longest neurite length, Nrn1, p-AkT, and Bcl-2 protein expression and had much lower Bax, Caspase-3, and Cleaved Caspase-3 protein expression. Nrn1 is a target gene of miR-194. miR-194 inhibited apoptosis of Aβ1–42-transduced hippocampal neurons by inhibiting Nrn1 and decreasing PI3K/AkT signaling pathway activity.
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Li, Shan, Lihai Zhang, Shuhua Li, Hengyi Zhao, and Yonggang Chen. "Curcumin suppresses the progression of gastric cancer by regulating circ_0056618/miR-194-5p axis." Open Life Sciences 16, no. 1 (January 1, 2021): 937–49. http://dx.doi.org/10.1515/biol-2021-0092.
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Abstract Curcumin has been demonstrated to be an anti-tumor agent in many types of cancers, including gastric cancer (GC). However, the molecular mechanisms by which curcumin performs its anti-tumor effects remain elusive. circ_0056618 and miR-194-5p are reported to be involved in GC progression, but their relationships with curcumin are unclear. In this study, circ_0056618 was elevated, and miR-194-5p was reduced in GC tissues and cells. Curcumin treatment led to a decrease in circ_0056618 level in GC cells. Overexpression of circ_0056618 promoted cell proliferation, migration, and invasion and suppressed cell cycle arrest and apoptosis in curcumin-treated GC cells. Moreover, miR-194-5p was identified as the target of circ_0056618, and its expression in GC cells increased after curcumin treatment. Overexpression of miR-194-5p reversed the promotional effect of circ_0056618 on cell progression in curcumin-treated GC cells. Additionally, curcumin treatment repressed the tumorigenesis of GC in vivo through regulating circ_0056618. Curcumin treatment delayed the development of GC partly through decreasing circ_0056618 and increasing miR-194-5p.
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D’Angelo, Edoardo, Carlo Zanon, Francesca Sensi, Maura Digito, Massimo Rugge, Matteo Fassan, Marco Scarpa, Salvatore Pucciarelli, Donato Nitti, and Marco Agostini. "miR-194 as predictive biomarker of responsiveness to neoadjuvant chemoradiotherapy in patients with locally advanced rectal adenocarcinoma." Journal of Clinical Pathology 71, no. 4 (September 4, 2017): 344–50. http://dx.doi.org/10.1136/jclinpath-2017-204690.
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AimsCurative surgery remains the primary form of treatment for locally advanced rectal cancer (LARC). Recent data support the use of preoperative chemoradiotherapy (pCRT) to improve the prognosis of LARC with a significant reduction of local relapse and an increase of overall survival. Unfortunately, only 20% of the patients with LARC present complete pathological response after pCRT, whereas in 20%–40%, the response is poor or absent.MethodsWe investigated the expression level of miR-194 in n=38 patients with LARC using our public microRNA (miRNA) expression dataset. miR-194 expression was further validated by real-time quantitative PCR (qRT-PCR) and in situ hybridisation (ISH). Protein–protein interaction network and pathway enrichment analysis were performed on miR-194 targets.Results and discussionUsing biopsy samples collected at diagnosis, mir-194 was significantly upregulated in patients responding to treatment (p value=0.016). The data was confirmed with qRT-PCR (p value=0.0587) and ISH (p value=0.026). Protein–protein interaction network and pathway enrichment analysis reveal a possible mechanism of susceptibility to pCRT involving Wnt pathway via its downstream mediator TRAF6. Finally, we interrogated the Comparative Toxicogenomics Database database in order to identify those chemical compounds able to mimic the biological effects of miR-194 as new possible therapeutic option in LARC treatment. The present study combining miRNA expression profiling with integrative computational biology identified miR-194 as predictive biomarker of response to pCRT. Using known and predicted drug mechanism of action, we then identified possible chemical compounds for further in vitro validation.
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Khella, Heba W. Z., Marize Bakhet, Ghassan Allo, Michael A. S. Jewett, Andrew Girgis, Georg A. Bjarnason, and George M. Yousef. "Supression of tumor progression and metastasis in renal cell carcinoma by miR-192, miR-194, and miR-215." Journal of Clinical Oncology 31, no. 6_suppl (February 20, 2013): 385. http://dx.doi.org/10.1200/jco.2013.31.6_suppl.385.
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385 Background: miRNAs play a crucial rule in tumor progression and metastasis. We previously identified miR-192, miR-194 and miR-215 to be down-regulated in metastatic compared to primary clear cell renal cell carcinoma (ccRCC). In this work, we examine the role of miR-192, miR-194, and miR-215 in RCC progression and aggressiveness. Methods: We examined the role of these three miRNAs on tumor cell migration and invasion abilities using RCC cell line models. We performed target prediction analysis and experimentally validated the targets using independent approaches. In addition, we examined the clinical utility of miR-215 as a potential prognostic marker in RCC by measuring miR-215 expression using qRT-PCR in 61 formalin-fixed paraffin-embedded tissues from primary ccRCC and correlated the expression levels with clinical outcome. Results: Restoration of miR-192, miR-194, and miR-215 expression decreased cell migration and invasion in RCC cell lines. Target prediction analysis identified three potential targets of these miRNAs; MDM2, TYMS, and SIP1/ZEB2. We validated the miRNA-target interaction experimentally using three approaches. First by measuring the effect of miRNA overexpression on mRNA and protein levels of the predicted target, then by measuring the effect of miRNA overexpression on a luciferase signal of a vector containing the 3’UTR of the predicted target, and finally, by validating these interactions in vivoby examining the presence of an inverse correlation between miRNA changes and the expression levels of their targets on clinical specimens. In 61 patients with resected ccRCC tumors, we found that low miR-215 expression in the primary was associated with a significantly reduced recurrence-free survival. (26.4 vs. 49.2 months, respectively, p = 0.0320). Conclusions: Our analysis showed that miR-192, miR-194, and miR-215 are involved in RCC metastasis and that miR-215 predicts for recurrence in patients with resected RCC. Our findings pave the way to the clinical use of miRNAs as prognostic markers and potential therapeutic targets.
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Kito, Naoko, Kosuke Endo, Masahiro Ikesue, Huachun Weng, and Naoharu Iwai. "miRNA Profiles of Tubular Cells: Diagnosis of Kidney Injury." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/465479.
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MicroRNAs (miRNAs) are small noncoding RNAs of 18–23 nucleotides that regulate gene expression. Recently, plasma miRNAs have been investigated as biomarkers for various physiological and pathological conditions. The present study details the conserved miRNA expression profiles of tubular tissues, and discusses whether they could be used to distinguish between proximal tubule injury, diagnose acute kidney injury (AKI), and the early-stage renal tubular dysfunction. miRNA expression was assessed with miRNA array and real-time reverse transcription polymerase chain reaction using the TaqMan system. The expression profiles of miR-200a/b/c, miR-145, miR-192, miR-194, miR-216a/b, miR-217, and miR-449a in human and rat tubular tissues such as the kidneys, lung, small intestine, and various exocrine glands were adequate for discriminating tubular tissues. In the kidney, miR-192 and miR-194 were highly expressed, whereas miR-145 and miR-449a were absent. miR-145 and miR-449a were relatively specifically expressed in small intestine and lung, respectively. Therefore, the combined levels of miR-200a/b/c, miR-192, and miR-194 in plasma were very useful in diagnosing AKI induced by contact freezing in mice. Moreover, urinary miR-200a levels were useful for the diagnosis of renal tubular dysfunction in Dahl salt-sensitive rat with high salt administration. Our results indicate that miRNA expression profiles are useful as biomarkers for identification of various kidney injuries.
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Torres, L. F., B. Cogliati, and R. Otton. "Green Tea Prevents NAFLD by Modulation of miR-34a and miR-194 Expression in a High-Fat Diet Mouse Model." Oxidative Medicine and Cellular Longevity 2019 (December 4, 2019): 1–18. http://dx.doi.org/10.1155/2019/4168380.
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Background/Aims. Nonalcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of metabolic syndrome. It is currently the most common chronic liver disease with complex pathogenesis and challenging treatment. Here, we investigated the hepatoprotective role of green tea (GT) and determined the involvement of miRNAs and its mechanism of action. Methods. Male C57Bl/6 mice were fed with a high-fat diet for 4 weeks. After this period, the animals received gavage with GT (500 mg/kg body weight) over 12 weeks (5 days/week). HepG2 cell lines were transfected with miR-34a or miR-194 mimetics and inhibitors to validate the in vivo results or were treated with TNF-α to evaluate miRNA regulation. Results. GT supplementation protects against NAFLD development by altering lipid metabolism, increasing gene expression involved in triglycerides and fatty acid catabolism, and decreasing uptake and lipid accumulation. This phenotype was accompanied by miR-34a downregulation and an increase in their mRNA targets Sirt1, Pparα, and Insig2. GT upregulated hepatic miR-194 by inhibiting TNF-α action leading to a decrease in miR-194 target genes Hmgcs/Apoa5. Conclusion. Our study identified for the first time that the beneficial effects of GT in the liver can be due to the modulation of miRNAs, opening new perspectives for the treatment of NAFLD focusing on epigenetic regulation of miR-34a and miR-194 as green tea targets.
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Jia, Yijie, Meiping Guan, Zongji Zheng, Qian Zhang, Chuan Tang, Wenwei Xu, Zhizhou Xiao, Ling Wang, and Yaoming Xue. "miRNAs in Urine Extracellular Vesicles as Predictors of Early-Stage Diabetic Nephropathy." Journal of Diabetes Research 2016 (2016): 1–10. http://dx.doi.org/10.1155/2016/7932765.
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Background. miR-192, miR-194, and miR-215 are enriched in the kidney and play roles in the pathogenesis of diabetic nephropathy (DN). Extracellular vesicles (EVs) can be detected in body fluids and may serve as disease biomarkers.Methods. Eighty type 2 diabetes patients with normoalbuminuria (n=30), microalbuminuria (n=30), or macroalbuminuria (n=20), as well as 10 healthy controls, were enrolled in this study. Real-time PCR was used to evaluate urinary EV miRNAs expression.Results. The miR-192 levels were significantly higher than the miR-194 and miR-215 levels in urine EVs and all three miRNAs were significantly increased in the microalbuminuric group compared with the normoalbuminuric and control subjects but were decreased in the macroalbuminuric group. In patients with normoalbuminuria and microalbuminuria, miR-192 was positively correlated with albuminuria (r=0.357,P=0.005) levels and transforming growth factor- (TGF-)β1 (r=0.356,P=0.005) expression. Receiver operating characteristic (ROC) curve analysis revealed that miR-192 was better than miR-194 and miR-215 in discriminating the normoalbuminuric group from the microalbuminuric group. Exposure of human renal tubular epithelial cells to high glucose increased the expression of both miRNAs in cellular supernatant EVs, indicating a potential source.Conclusion. These results suggest the potential use of urinary EV miR-192 as a biomarker of the early stage of DN.
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van der Sijde, Fleur, Marjolein Y. V. Homs, Marlies L. van Bekkum, Thierry P. P. van den Bosch, Koop Bosscha, Marc G. Besselink, Bert A. Bonsing, et al. "Serum miR-373-3p and miR-194-5p Are Associated with Early Tumor Progression during FOLFIRINOX Treatment in Pancreatic Cancer Patients: A Prospective Multicenter Study." International Journal of Molecular Sciences 22, no. 20 (October 9, 2021): 10902. http://dx.doi.org/10.3390/ijms222010902.
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In this study, we explored the predictive value of serum microRNA (miRNA) expression for early tumor progression during FOLFIRINOX chemotherapy and its association with overall survival (OS) in patients with pancreatic ductal adenocarcinoma (PDAC). A total of 132 PDAC patients of all disease stages were included in this study, of whom 25% showed progressive disease during FOLFIRINOX according to the RECIST criteria. MiRNA expression was analyzed in serum collected before the start and after one cycle of chemotherapy. In the discovery cohort (n = 12), a 352-miRNA RT-qPCR panel was used. In the validation cohorts (total n = 120), miRNA expression was detected using individual RT-qPCR miRNA primers. Before the start of FOLFIRINOX, serum miR-373-3p expression was higher in patients with progressive disease compared to patients with disease control after FOLFIRINOX (Log2 fold difference (FD) 0.88, p = 0.006). MiR-194-5p expression after one cycle of FOLFIRINOX was lower in patients with progressive disease (Log2 FD −0.29, p = 0.044). Both miRNAs were predictors of early tumor progression in a multivariable model including disease stage and baseline CA19-9 level (miR-373-3p odds ratio (OR) 3.99, 95% CI 1.10–14.49; miR-194-5p OR 0.91, 95% CI 0.83–0.99). MiR-373-3p and miR-194-5p did not show an association with OS after adjustment for disease stage, baseline CA19-9, and chemotherapy response. In conclusion, high serum miR-373-3p before the start and low serum miR-194-5p after one cycle are associated with early tumor progression during FOLFIRINOX.
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Bose, Sudeep, Tracy E. Tholanikunnel, Adrian Reuben, Baby G. Tholanikunnel, and Eleanor K. Spicer. "Regulation of nucleolin expression by miR-194, miR-206, and HuR." Molecular and Cellular Biochemistry 417, no. 1-2 (May 25, 2016): 141–53. http://dx.doi.org/10.1007/s11010-016-2721-2.
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Li, Jun, Haoyu Gao, Beibei Chen, Li Li, Qianqing Wang, and Zhihui Gao. "lncRNA DARS-AS1 Modulates TSPAN1-Mediated ITGA2 Hypomethylation by Interaction with miR-194-5p Thus Promoting Ovarian Cancer Progression." Stem Cells International 2022 (September 22, 2022): 1–14. http://dx.doi.org/10.1155/2022/4041550.
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Objective. Ovarian cancer (OC) is usually called the “silent killer” due to its asymptomatic characteristics until advanced stages, thus being a significant threat to female health worldwide. In this work, we characterized an oncogenic DARS-AS1 role in OC. Methods. The aggressiveness behaviors of the OC cell model were examined by CCK-8 assay, transwell invasion assay, flow cytometry, and immunoblotting analysis of apoptosis-related proteins. Interactions of miR-194-5p with lncRNA DARS-AS1 or TSPAN1 and of TSPAN1 with ITGA2 were validated by using a luciferase activity assay and chromatin immunoprecipitation (ChIP) assay. Results. The OC cell model exhibited overexpressed lncRNA DARS-AS1 compared to normal cells. lncRNA DARS-AS1 knockdown led to reduced OC cell growth and metastasis while inducing the apoptosis in the OC cell model. lncRNA DARS-AS1 positively regulated TSPAN1 expression by binding with miR-194-5p and TSPAN1-mediated ITGA2 hypomethylation in OC cells. Further rescue function studies demonstrated that lncRNA DARS-AS1 affected OC cell viability, migration, invasion, and apoptosis ability by modulating miR-194-5p and TSPAN1 expressions. Conclusion. Our work demonstrates that lncRNA DARS-AS1 promotes OC progression by modulating TSPAN1 and ITGA2 hypomethylation by binding with miR-194-5p.
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Xiang, Yangfeng, Wendong Wang, Jialei Gu, and Jinbiao Shang. "Circular RNA VANGL1 Facilitates Migration and Invasion of Papillary Thyroid Cancer by Modulating the miR-194/ZEB1/EMT Axis." Journal of Oncology 2022 (March 8, 2022): 1–8. http://dx.doi.org/10.1155/2022/4818651.
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Circular RNAs (circRNAs) are often aberrantly expressed in human tumors and also serve a critical regulatory role in papillary thyroid cancer (PTC). The aim of this study is to investigate the expression pattern and biological role of circVANGL1 in PTC. The results revealed that circVANGL1 was significantly upregulated in human PTC samples. In addition, high circVANGL1 expression was closely associated with adverse clinical parameters of PTC patients. Our in vitro experiments further indicated that the knockdown of circVANGL1 using siRNA obviously repressed migration, proliferation, EMT, and invasion of PTC cells, while opposite effects were induced by its overexpression. We further noted that circVANGL1 could interact with miR-194 directly in PTC, and serve as a ceRNA to regulate ZEB1 function. Moreover, miR-194 inhibition markedly abrogated the effects of circVANGL1 knockdown in PTC cells. Therefore, our results provide convincing evidence that circVANGL1 may exert oncogenic effects in PTC, partly via regulating the miR-194/ZEB1 axis.
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Zhai, Haiyan, Mihriban Karaayvaz, Peixin Dong, Noriaki Sakuragi, and Jingfang Ju. "Prognostic significance of miR-194 in endometrial cancer." Biomarker Research 1, no. 1 (2013): 12. http://dx.doi.org/10.1186/2050-7771-1-12.
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Dell'Aversana, C., C. Giorgio, L. D'Amato, G. Lania, F. Matarese, S. Saeed, A. Di Costanzo, et al. "miR-194-5p/BCLAF1 deregulation in AML tumorigenesis." Leukemia 31, no. 11 (February 20, 2017): 2315–25. http://dx.doi.org/10.1038/leu.2017.64.
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Bay, Ali, Enes Coskun, Serdar Oztuzcu, Sercan Ergun, Fatih Yilmaz, and Elif Aktekin. "EVALUATION OF THE PLASMA MICRO RNA EXPRESSION LEVELS IN SECONDARY HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS." Mediterranean Journal of Hematology and Infectious Diseases 5, no. 1 (November 4, 2013): e2013066. http://dx.doi.org/10.4084/mjhid.2013.066.
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Background: Hemophagocytic lymphohistiocytosis (HLH) is a life threatening hyper inflammatory disease. Micro RNAs (miRNA) are about 22 nucleotide-long, small RNAs encoded with genes, and they have regulatory functions in immune response. Objective: To determine the miRNA expression levels of 11 secondary HLH patients, we evaluated the associations of miRNA levels with pathogenesis, clinical presentation, and prognosis of the disease. Patients and Methods: Patients who were diagnosed with secondary HLH from January 2011 to December 2012 were included in this study. We profiled the expressions of 379 miRNAs in plasma of both HLH patients and healthy controls. Patients were evaluated regarding with age, clinical findings, miRNA expresions, laboratory data, treatment, and prognosis, by using descriptive statistics. Results: A total of 11 secondary HLH patients and 11 healthy children were included in this study. miR-205-5p was expressed in all case and controls and expression level of miR-205-5p was found 6.21 fold higher than control group (p=0.01). We detected the second highest expression percent in miR-194-5p with 81% of cases and controls. Expression level of miR-194-5p was found to have 163 fold higher than controls (p= 0.009). miR-30c-5p showed 77% expression percent in cases and controls together. The expression level of this miRNA was detected 9 fold decreased in HLH patients compared to healthy children (p= 0.031). Conclusion: We showed that miR-205-5p, miR-194-5p and miR-30c-5p could be useful plasma biomarkers for HLH. Further research is needed in larger and homogenous study groups, especially for these miRNAs as biomarkers for HLH.
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de la Cruz-Ojeda, Patricia, Tobias Schmid, Loreto Boix, Manuela Moreno, Víctor Sapena, Juan M. Praena-Fernández, Francisco J. Castell, et al. "miR-200c-3p, miR-222-5p, and miR-512-3p Constitute a Biomarker Signature of Sorafenib Effectiveness in Advanced Hepatocellular Carcinoma." Cells 11, no. 17 (August 28, 2022): 2673. http://dx.doi.org/10.3390/cells11172673.
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Background: Sorafenib constitutes a suitable treatment alternative for patients with advanced hepatocellular carcinoma (HCC) in whom atezolizumab + bevacizumab therapy is contraindicated. The aim of the study was the identification of a miRNA signature in liquid biopsy related to sorafenib response. Methods: miRNAs were profiled in hepatoblastoma HepG2 cells and tested in animal models, extracellular vesicles (EVs), and plasma from HCC patients. Results: Sorafenib altered the expression of 11 miRNAs in HepG2 cells. miR-200c-3p and miR-27a-3p exerted an anti-tumoral activity by decreasing cell migration and invasion, whereas miR-122-5p, miR-148b-3p, miR-194-5p, miR-222-5p, and miR-512-3p exerted pro-tumoral properties by increasing cell proliferation, migration, or invasion, or decreasing apoptosis. Sorafenib induced a change in EVs population with an increased number of larger EVs, and promoted an accumulation of miR-27a-3p, miR-122-5p, miR-148b-3p, miR-193b-3p, miR-194-5p, miR-200c-3p, and miR-375 into exosomes. In HCC patients, circulating miR-200c-3p baseline levels were associated with increased survival, whereas high levels of miR-222-5p and miR-512-3p after 1 month of sorafenib treatment were related to poor prognosis. The RNA sequencing revealed that miR-200c-3p was related to the regulation of cell growth and death, whereas miR-222-5p and miR-512-3p were related to metabolic control. Conclusions: The study showed that Sorafenib regulates a specific miRNA signature in which miR-200c-3p, miR-222-5p, and miR-512-3p bear prognostic value and contribute to treatment response.
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Domsa, Elena Maria, Ioana Berindan-Neagoe, Livia Budisan, Cornelia Braicu, Ioana Para, Alina Ioana Tantau, Olga Hilda Orasan, et al. "Expression of Selected Genes and Circulating microRNAs in Patients with Celiac Disease." Medicina 58, no. 2 (January 25, 2022): 180. http://dx.doi.org/10.3390/medicina58020180.
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Background and Objectives: Celiac disease (CD) is an immune-mediated enteropathy with characteristic intestinal alterations. CD occurs as a chronic inflammation secondary to gluten sensitivity in genetically susceptible individuals. Until now, the exact cause of the disease has not been established, which is why new studies have appeared that address the involvement of various genes and microRNAs (miRNAs) in the pathogenesis. The aim of the study is to describe the expression of selected genes (Wnt family member 3, WNT3; Wnt family member 11, WNT11; tumor necrosis factor alpha, TNFα; mitogen-activated protein kinase 1, MAPK1; AKT serine/threonine kinase 3, AKT3; phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, PIK3CA; and cyclin D1, CCND1) and miRNAs (miR-192-5p, miR-194-5p, miR-449a and miR-638) in adult patients with CD. Materials and Methods: In total, 15 patients with CD at diagnosis (newly diagnosed), 33 patients on a gluten-free diet (GFD) for at least 1 year and 10 controls (control) were prospectively included. Blood samples were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). Results: The results show that TNFα, MAPK1 and CCND1 were significantly overexpressed (p = 0.0249, p = 0.0019 and p = 0.0275, respectively) when comparing the newly diagnosed group to the controls. The other genes studied in CD patients were mostly with high values compared to controls, without reaching statistical significance. Among the miRNAs, the closest to a statistically significant value was miR-194-5p when the newly diagnosed group versus control (p = 0.0510) and GFD group versus control (p = 0.0671) were compared. The DIANA and miRNet databases identified significant functional activity for miR-449a and miR-192-5p and an interconnection of miR-194-5p and miR-449a with CCND1. Conclusions: In conclusion, genes and circulating miRNAs require further studies as they could represent important biomarkers in clinical practice.
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Wang, Tongfei, Wei Li, Haitao Li, and Weina Li. "Dysregulation of exosomal miR-192 and miR-194 expression in lung adenocarcinoma patients." Saudi Journal of Biological Sciences 28, no. 3 (March 2021): 1561–68. http://dx.doi.org/10.1016/j.sjbs.2021.01.013.
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Kalabat, Dalia Y., Allison Vitsky, Wesley Scott, Erick Kindt, Kyle Hayes, Annette John-Baptiste, Wenhu Huang, and Amy H. Yang. "Identification and Evaluation of Novel MicroRNA Biomarkers in Plasma and Feces Associated with Drug-induced Intestinal Toxicity." Toxicologic Pathology 45, no. 2 (July 11, 2016): 302–20. http://dx.doi.org/10.1177/0192623316644992.
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Gastrointestinal toxicity is dose limiting with many therapeutic and anticancer agents. Real-time, noninvasive detection of markers of toxicity in biofluids is advantageous. Ongoing research has revealed microRNAs as potential diagnostic and predictive biomarkers for the detection of select organ toxicities. To study the potential utility of microRNA biomarkers of intestinal injury in a preclinical toxicology species, we evaluated 3 rodent models of drug-induced intestinal toxicity, each with a distinct mechanism of toxicity. MiR-215 and miR-194 were identified as putative intestinal toxicity biomarkers. Both were evaluated in plasma and feces and compared to plasma citrulline, an established intestinal injury biomarker. Following intestinal toxicant dosing, microRNA changes in feces and plasma were detected noninvasively and correlated with histologic evidence of intestinal injury. Fecal miR-215 and miR-194 levels increased, and plasma miR-215 decreased in a dose- and time-dependent manner. Dose-dependent decreases in plasma miR-215 levels also preceded and correlated positively with plasma citrulline modulation, suggesting miR-215 is a more sensitive biomarker. Moreover, during the drug-free recovery phase, plasma miR-215 returned to predose levels, supporting a corresponding recovery of histologic lesions. Despite limitations, this study provides preliminary evidence that select microRNAs have the potential to act as noninvasive, sensitive, and quantitative biomarkers of intestinal injury.
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Wang, Li-ping, Yu-zhen Gao, Bin Song, Guo Yu, Hui Chen, Zhen-wen Zhang, Cai-feng Yan, Yun-long Pan, and Xiao-yan Yu. "MicroRNAs in the Progress of Diabetic Nephropathy: A Systematic Review and Meta-Analysis." Evidence-Based Complementary and Alternative Medicine 2019 (March 7, 2019): 1–9. http://dx.doi.org/10.1155/2019/3513179.
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Background. We conducted a systematic review and meta-analysis of existing literature to evaluate the different outcomes of microRNAs (miRNAs) in diabetic nephropathy (DN), including urinary albumin excretion rates, urinary albumin creatinine rates, glomerular filtration rate, HbAc1, and creatinine.Methods. Electronic databases including PUBMED, MEDLINE, and EMBASE were searched for eligible publications to July 2018. The following comparisons between treatment groups were included: normal group versus DN group; control group versus micro/macroalbuminuria group.Results. Twelve eligible studies that included 2500 participants were finally recruited in this meta-analysis. Fifteen miRNAs (miRNA-21, miRNA-181b, miRNA-194, miRNA-30, miRNA-215, and others) were upregulated whereas seven miRNAs (miRNA-26a, miRNA-126, miRNA-424, miRNA-574-3p, miR-223, miR-155, and miR-192) were downregulated in the DN group compared with control groups. The miR-133b, miR-342, miR-30, miR-192, miR-194, and miR-215 were significantly correlated in urinary albumin excretion rates (r=0.33, 95% CI= 0.26-0.39). miR-192, miR-217, miR-15b, miR-34a, and miR-636 were correlated with urinary albumin creatinine rates (r=0.69; 95% CI=0.12-0.92), while miR-133b, miR-345, miR-33, miR-326, miR-574-3p, miR-126, miR-217, miR-15b, miR-34a, and miR-636 were significantly correlated with HbAc1 (r =0.23, 95% CI = 0.15-0.31). There were twelve miRNAs that were closely related to the glomerular filtration rate (r=0.28, 95% CI =0.21-0.34). Creatinine (r=0.33, 95% CI = 0.22-0.40) was significantly different between normal and DN groups.Conclusions. The meta-analysis acquired the correlations between miRNAs and outcomes including UAER, UACR, eGFR, HbAc1, and creatinine in DN. It suggested that miRNAs may participate in the pathogenesis of DN process.
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Zhang, Q., T. Wei, K. Shim, K. Wright, K. Xu, H. L. Palka-Hamblin, A. Jurkevich, and S. Khare. "Atypical role of sprouty in colorectal cancer: sprouty repression inhibits epithelial–mesenchymal transition." Oncogene 35, no. 24 (October 5, 2015): 3151–62. http://dx.doi.org/10.1038/onc.2015.365.
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Abstract Sprouty (SPRY) appears to act as a tumor suppressor in cancer, whereas we demonstrated that SPRY2 functions as a putative oncogene in colorectal cancer (CRC) (Oncogene, 2010, 29: 5241–5253). We investigated the mechanisms by which SPRY regulates epithelial–mesenchymal transition (EMT) in CRC. SPRY1 and SPRY2 mRNA transcripts were significantly upregulated in human CRC. Suppression of SPRY2 repressed AKT2 and EMT-inducing transcription factors and significantly increased E-cadherin expression. Concurrent downregulation of SPRY1 and SPRY2 also increased E-cadherin and suppressed mesenchymal markers in colon cancer cells. An inverse expression pattern between AKT2 and E-cadherin was established in a human CRC tissue microarray. SPRY2 negatively regulated miR-194-5p that interacts with AKT2 3′ untranslated region. Mir-194 mimics increased E-cadherin expression and suppressed cancer cell migration and invasion. By confocal microscopy, we demonstrated redistribution of E-cadherin to plasma membrane in colon cancer cells transfected with miR-194. Spry1 −/− and Spry2 −/− double mutant mouse embryonic fibroblasts exhibited decreased cell migration while acquiring several epithelial markers. In CRC, SPRY drive EMT and may serve as a biomarker of poor prognosis.
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Hu, Lingmin, Jing Han, Fangxiu Zheng, Hongxia Ma, Jiaping Chen, Yue Jiang, and Hua Jiang. "Early Second-Trimester Serum MicroRNAs as Potential Biomarker for Nondiabetic Macrosomia." BioMed Research International 2014 (2014): 1–6. http://dx.doi.org/10.1155/2014/394125.
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Background. Macrosomia has become a worldwide problem with the rapid economic growth in the past few years. However, the detailed mechanism of how the macrosomia happened remains unknown. Growing evidence indicates that miRNAs are involved in maintaining metabolic homeostasis. We hypothesized that serum miRNAs are potential biomarkers for macrosomia.Methods. We performed miRNAs profiling using TLDA chips in the discovery phase in two pooled samples from 30 cases and 30 controls, respectively. Individual qRT-PCR was conducted for the discovery phase samples. To confirm the results, we detected the miRNAs which were differentially expressed in the microarray assays and individual qRT-PCR in external validation phase with another 30 cases and 30 controls.Results. In the discovery stage, miR-194 and miR-376a expression levels were significantly different between macrosomia group and controls (P=0.048for miR-194 andP=0.018for miR-376a, resp.). Further evaluation of the two miRNAs on a total of 120 serum samples showed that the miR-376a remains significantly lower in macrosomia (P=0.032). Receiver operating characteristic curve analyses showed that the area under curve for miR-376a was 67.8% (sensitivity = 96.7% and specificity = 40.0%).Conclusions. Serum miR-376a may serve as a potential noninvasive biomarker in detecting macrosomia.
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Fan, Jingjing, Yong Chen, Wei Zhang, Xiaoying Zhou, Xue Bai, Caifang Chang, Yongping Han, and Jinlu Liu. "Identification of the Hub Genes and Potential Regulation Network in Chronic Hepatitis B via Bioinformatics Analysis." Disease Markers 2022 (September 23, 2022): 1–12. http://dx.doi.org/10.1155/2022/6113807.
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Background. Chronic hepatitis B (CHB) is a serious infectious disease which is induced by hepatitis B virus (HBV) infection. This project was conducted to reveal the potential mechanism in CHB development via analyzing the public clinical data. Methods. GSE33857 and GSE110217, obtained from the GEO database, were used for bioinformatics excavation. Briefly, the raw data of GSE33857 and GSE110217 were analyzed with the GEO2R, and then the expressed matrix files were generated. The matrix files was visualized as heat map with R software. The targets of the miRNAs were analyzed with the miRDIP database. The functional annotation and pathway enrichment were performed using “clusterProfiler” package in R software. The STRING database was utilized to analyze the interaction of the DEGs, and the PPI and miRNA-mRNA network were established according to the related results. Results. 93 downregulated genes and 17 upregulated genes in GES33857, and 111 downregulated and 40 upregulated genes in GSE110217 were identified as the hub nodes. The targets of the DEGs in the datasets were enriched in PI3K/AKT and MAPK pathways and associated with transcriptional regulation. Moreover, PPI and miRNA-mRNA networks were also established with the DEGs and related targets in the datasets. miR-122-5p, miR-125b-5p, miR-136-5p, miR-194-5p, miR-139-5p, miR-140-5p, miR-181a-5p, and miR-29b-3p were identified as the potential biomarkers in CHB. Conclusion. Eight miRNAs, including miR-122-5p, miR-125b-5p, miR-136-5p, miR-194-5p, miR-139-5p, miR-140-5p, miR-181a-5p, and miR-29b-3p, were identified as the potential biomarkers in CHB, and the PPI and miRNA-mRNA networks were also established.
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Dell'Aversana, C., C. Giorgio, L. D'Amato, G. Lania, F. Matarese, S. Saeed, A. Di Costanzo, et al. "Erratum: miR-194-5p/BCLAF1 deregulation in AML tumorigenesis." Leukemia 32, no. 2 (December 22, 2017): 573. http://dx.doi.org/10.1038/leu.2017.310.
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Della Vittoria Scarpati, Giuseppina, Enrica Calura, Mariacristina Di Marino, Chiara Romualdi, Luca Beltrame, Umberto Malapelle, Giancarlo Troncone, et al. "Analysis of Differential miRNA Expression in Primary Tumor and Stroma of Colorectal Cancer Patients." BioMed Research International 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/840921.
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Microarray technology was used to profile miRNA expression in primary tumor and stromal tissue from paraffin embedded material of 51 patients with colorectal cancer. 26 miRNAs resulted differentially expressed with at least 2-fold change in tumor tissue with respect to stroma (16 more expressed in the tumor and 10 more expressed in the stroma). 10/26 were confirmed as differentially expressed at qRTPCR: miR-200c-3p, miR-141-3p, miR-200b-3p, miR-200a-3p, miR-1246, miR-92a-3p, miR-194-5p, miR-192-5p, miR-3651-5p, and miR-574-3p. No significant association was found between miRNA expressions and stage at diagnosis, site of primary tumor, first site of metastasis, progression-free, or overall survival.
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Zhang, Lemeng, Jianhua Chen, Tianli Cheng, Hua Yang, Changqie Pan, and Haitao Li. "Identification of Differentially Expressed Genes and miRNAs Associated with Esophageal Squamous Cell Carcinoma by Integrated Analysis of Microarray Data." BioMed Research International 2020 (July 2, 2020): 1–16. http://dx.doi.org/10.1155/2020/1980921.
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To identify candidate key genes and miRNAs associated with esophageal squamous cell carcinoma (ESCC) development and prognosis, the gene expression profiles and miRNA microarray data including GSE20347, GSE38129, GSE23400, and GSE55856 were downloaded from the Gene Expression Omnibus (GEO) database. Clinical and survival data were retrieved from The Cancer Genome Atlas (TCGA). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of differentially expressed genes (DEGs) was analyzed via DAVID, while the DEG-associated protein-protein interaction network (PPI) was constructed using the STRING database. Additionally, the miRNA target gene regulatory network and miRNA coregulatory network were constructed, using the Cytoscape software. Survival analysis and prognostic model construction were performed via the survival (version 2.42-6) and rbsurv R packages, respectively. The results showed a total of 2575, 2111, and 1205 DEGs, and 226 differentially expressed miRNAs (DEMs) were identified. Pathway enrichment analyses revealed that DEGs were mainly enriched in 36 pathways, such as the proteasome, p53, and beta-alanine metabolism pathways. Furthermore, 448 nodes and 1144 interactions were identified in the PPI network, with MYC having the highest random walk score. In addition, 7 DEMs in the microarray data, including miR-196a, miR-21, miR-205, miR-194, miR-103, miR-223, and miR-375, were found in the regulatory network. Moreover, several reported disease-related miRNAs, including miR-198a, miR-103, miR-223, miR-21, miR-194, and miR-375, were found to have common target genes with other DEMs. Survival analysis revealed that 85 DEMs were related to prognosis, among which hsa-miR-1248, hsa-miR-1291, hsa-miR-421, and hsa-miR-7-5p were used for a prognostic survival model. Taken together, this study revealed the important roles of DEGs and DEMs in ESCC development, as well as DEMs in the prognosis of ESCC. This will provide potential therapeutic targets and prognostic predictors for ESCC.
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Kinoo, Suman Mewa, Pragalathan Naidoo, Bhugwan Singh, Anil Chuturgoon, and Savania Nagiah. "Human Hepatocyte Nuclear Factors (HNF1 and LXRb) Regulate CYP7A1 in HIV-Infected Black South African Women with Gallstone Disease: A Preliminary Study." Life 13, no. 2 (January 18, 2023): 273. http://dx.doi.org/10.3390/life13020273.
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Female sex, high estrogen levels, aging, obesity, and dyslipidemia are some of the risk factors associated with gallstone formation. HIV-infected patients on combination antiretroviral therapy (cART) are more prone to hypercholesterolemia. Bile acid synthesis is initiated by cholesterol 7-alpha hydroxylase (CYP7A1) and regulated by hepatocyte nuclear factors (HNF1α, HNF4α, and LXRb). The aim of this study was to evaluate the expression of HNF1α, HNF4α, LXRb, and miRNAs (HNF4α specific: miR-194-5p and miR-122*_1) that regulate CYP7A1 transcription in HIV-infected Black South African women on cART and presenting with gallstones relative to HIV-negative patients with gallstone disease. Females (n = 96) presenting with gallstone disease were stratified based on HIV status. The gene expression of CYP7A1, HNF1α, HNF4α, LXRb, miR-194-5p, and miR-122*_1 was determined using RT-qPCR. Messenger RNA and miRNA levels were reported as fold change expressed as 2−ΔΔCt (RQ min; RQ max). Fold changes >2 and <0.5 were considered significant. HIV-infected females were older in age (p = 0.0267) and displayed higher low-density lipoprotein cholesterol (LDL-c) (p = 0.0419), CYP7A1 [2.078-fold (RQ min: 1.278; RQ max: 3.381)], LXRb [2.595-fold (RQ min: 2.001; RQ max: 3.000)], and HNF1α [3.428 (RQ min: 1.806; RQ max: 6.507] levels. HNF4α [0.642-fold (RQ min: 0.266; RQ max: 1.55)], miR-194-5p [0.527-fold (RQ min: 0.37; RQ max: 0.752)], and miR-122*_1 [0.595-fold (RQ min: 0.332; RQ max: 1.066)] levels were lower in HIV-infected females. In conclusion, HIV-infected women with gallstone disease displayed higher LDL-c levels and increased bile acid synthesis, which was evidenced by the elevated expression of CYP7A1, HNF1α, and LXRb. This could have been further influenced by cART and aging.
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Stunf Pukl, Spela. "Are miRNAs Dynamic Biomarkers in Keratoconus? A Review of the Literature." Genes 13, no. 4 (March 25, 2022): 588. http://dx.doi.org/10.3390/genes13040588.
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Aim: A review of miRNA (microRNA) profiling studies in keratoconus. Methods: Literature search strategy—PubMed central database, using miRNA or microRNA and keratoconus as keywords. Results: Eleven experimental or clinical studies on humans regarding miRNA and keratoconus, published in English between 2009 and 2020 were retrieved. Conclusion: The publications regarding the role of miRNAs in keratoconus are scarce and diverse but provide some valuable information about potential new mechanisms of keratoconus development and progression. The cornea expresses almost 300 different miRNAs, 18 of which are specific, and miR-184 is by far the most abundant, with expression restricted to central basal and suprabasal epithelial cells. Mutations in the seed region of MIR184 were proved to be rare and nonspecific in patients with isolated keratoconus. Overall, in keratoconus, a total of 29 miRNAs were upregulated, and 11 were downregulated. It appeared that miR-143-3p, miR-182-5p, and miR-92a-3p were highly expressed, while the miRNAs connected to cell–cell junction, cell division, and motor activity were downregulated. In less advanced forms, altered expression of four miRNAs—miR-151a-3p, miR-194-5p, miR-195-5p, miR-185-5p—was proved in the cone epithelium; in contrast, in advanced keratoconus, the expression of miR-151a-3p and miR-194-5p remained altered, changes in the expression of miR-195 and miR-185 were not reported, and the expression of miR-138-5p, miR-146b-5p, miR-28-5p, and miR-181a-2-3p was also altered in the corneal epithelium. Keratoconus is a dynamic process of corneal stromal thinning that might result from a dynamic miRNA expression in the corneal epithelium exposed to environmental and behavioral factors causing repetitive traumas. Further experimental studies are needed to prove this hypothesis.
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Nakaoka, Toshiaki, Yoshimasa Saito, Yuriko Shimamoto, Toshihide Muramatsu, Masaki Kimura, Yae Kanai, and Hidetsugu Saito. "Cluster microRNAs miR-194 and miR-215 suppress the tumorigenicity of intestinal tumor organoids." Cancer Science 108, no. 4 (April 2017): 678–84. http://dx.doi.org/10.1111/cas.13165.
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Pichiorri, Flavia, Sung-Suk Suh, Luciana De Luca, Cristian Taccioli, Don Benson, Craig Hofmeister, Rami Aqeilan, and Carlo M. Croce. "p53-Inducible Micrornas 192 and 215 Regulate p53 Expression and IGF1 Axis in Multiple Myeloma." Blood 114, no. 22 (November 20, 2009): 1973. http://dx.doi.org/10.1182/blood.v114.22.1973.1973.
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Abstract Abstract 1973 Poster Board I-996 Multiple myeloma (MM) is an incurable neoplastic disease of B cell origin, affecting 50,000 patients in the United States, occurring in approximately 16,000 new individuals each year. In MM, mutation or deletion of p53 is rarely detected at diagnosis, although both become more frequent in advanced disease. Therapeutic activation of p53 might therefore be particularly suitable for the treatment of MM. The discovery of microRNAs (miRNAs) has revealed a new level of regulation of protein expression. We have shown that an altered miRNA expression profile plays a role in the malignant transformation of plasma cells (PCs); we recently published the first comprehensive global microRNA expression profiles of MM, monoclonal gammopathy of undetermined significance (MGUS) and contrasted these expression patterns with that of normal plasma cells (PCs). Now we have used nutlin-3a, a recently developed small-molecule activator of p53, that efficiently disrupts the p53-MDM2 interaction, to profile a p53 miRNA activation pathway in the MM1s cell line. Results of the analysis have shown differential expression of 46 individual miRNAs after p53 activation, 14 showing up-regulation and 32 showing down-regulation. We confirmed our data by qRT-PCR in p53 wild type and mutated MM cell lines and in primary MM cells. Our results confirm published results; after p53 stabilization we found up-regulation of the miR-34a, but we also detected strong up-regulation of several other miRNAs. In fact we found that p53 induces two additional, mutually related clusters of miRNAs, leading to the up-regulation of miR-192, miR-194, and miR-215. The same miRNAs were detected at high levels in normal plasma cells (n.3) but were severely reduced in many untreated MM samples (n.22). Here we characterize the promoter and the p53 activation site for miR-192-194 cluster on chromosome 11(q13.1) but we have also confirmed the previous published p53 consensus site for miR-215-194 cluster on chromosome 1(q41) in multiple myeloma cells. Furthermore we found that miR-192 and its cousin miR-215 but not miR-194 can each contribute to enhanced CDKN1A/p21 levels, colony suppression, cell cycle arrest in multiple myeloma cells acting directly on p53 regulation. On the other hand, we define that IGF-1 and IGFR are direct targets of miR-192-215. In fact the re-expression of these miRNAs in multiple myeloma cells blocks their migration through both endothelial barriers and associated bone marrow stroma. Our data suggest that downstream signaling in the p53 pathway is functional in MM cells and able to induce miRNAs that play a pivotal role in cell cycle progression, mobility and invasive properties of these cells. These studies provide the basis for the development of new miRNA-targeted therapies for MM. Disclosures: No relevant conflicts of interest to declare.
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Jabandziev, Petr, Tatsuhiko Kakisaka, Julia Bohosova, Tereza Pinkasova, Lumir Kunovsky, Ondrej Slaby, and Ajay Goel. "MicroRNAs in Colon Tissue of Pediatric Ulcerative Pancolitis Patients Allow Detection and Prognostic Stratification." Journal of Clinical Medicine 10, no. 6 (March 23, 2021): 1325. http://dx.doi.org/10.3390/jcm10061325.
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Prevalence of inflammatory bowel disease has been on the rise in recent years, especially in pediatric populations. This study aimed to provide precise identification and stratification of pediatric patients with diagnosed ulcerative colitis (UC) according to the severity of their condition and the prediction for standard treatment according to the specific expression of candidate miRNAs. We enrolled consecutive, therapeutically naïve, pediatric UC patients with confirmed pancolitis. We examined formalin-fixed paraffin-embedded specimens of colonic tissue for the expression of 10 selected candidate miRNAs. We performed receiver operating characteristic curve analysis, using area under the curve and a logistic regression model to evaluate the diagnostic and predictive power of the miRNA panels. Sixty patients were included in the final analysis. As a control group, 18 children without macroscopic and microscopic signs of inflammatory bowel disease were examined. The combination of three candidate miRNAs (let-7i-5p, miR-223-3p and miR-4284) enabled accurate detection of pediatric UC patients and controls. A panel of four candidate miRNAs (miR-375-3p, miR-146a-5p, miR-223-3p and miR-200b-3p) was associated with severity of UC in pediatric patients and a combination of three miRNAs (miR-21-5p, miR-192-5p and miR-194-5p) was associated with early relapse of the disease. Nine patients out of the total were diagnosed with primary sclerosing cholangitis (PSC) simultaneously with ulcerative colitis. A panel of 6 candidate miRNAs (miR-142-3p, miR-146a-5p, miR-223-3p, let-7i-5p, miR-192-5p and miR-194-5p) identified those patients with PSC. Specific combinations of miRNAs are promising tools for potential use in precise disease identification and severity and prognostic stratification in pediatric patients with ulcerative pancolitis.
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Khella, H. W. Z., M. Bakhet, G. Allo, M. A. S. Jewett, A. H. Girgis, A. Latif, H. Girgis, I. Von Both, G. A. Bjarnason, and G. M. Yousef. "miR-192, miR-194 and miR-215: a convergent microRNA network suppressing tumor progression in renal cell carcinoma." Carcinogenesis 34, no. 10 (May 28, 2013): 2231–39. http://dx.doi.org/10.1093/carcin/bgt184.
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Zhang, Bao-Le, Fu-Lu Dong, Ting-Wen Guo, Xiao-He Gu, Lin-Yan Huang, and Dian-Shuai Gao. "MiRNAs Mediate GDNF-Induced Proliferation and Migration of Glioma Cells." Cellular Physiology and Biochemistry 44, no. 5 (2017): 1923–38. http://dx.doi.org/10.1159/000485883.
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Background/Aims: Glial cell line-derived neurotrophic factor (GDNF) is an important factor promoting invasive glioma growth. This study was performed to reveal a unique mechanism of glioma cell proliferation and migration. Methods: Human U251 glioma cells were used to screen the optimal GDNF concentration and treatment time to stimulate proliferation and migration. MicroRNA (MiRNA) expression profiles were detected by microarray and confirmed by real-time polymerase chain reaction (PCR). The target genes of differentially expressed miRNAs were predicted by miRWalk, and those targeted by multiple miRNAs were screened with Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. A regulatory miRNA network was constructed using ingenuity pathway analysis (IPA). Target gene expression of differentially expressed miRNAs was examined by real-time PCR or mRNA microarray. Results: The results show that 50 ng/mL GDNF for 24 h significantly promotes U251 glioma cell proliferation and migration (P < 0.05). Seven miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-629-5p, hsa-miR-3609, hsa-miR-183-5p, and hsa-miR-487b-3p) were significantly up-regulated after GDNF treatment (P < 0.05). These miRNAs are primarily involved in signal transduction, cell adhesion and cell cycle through mitogen-activated protein kinase (MAPK) signaling, focal adhesion and glioma signal pathways. Five of these miRNAs (hsa-miR-194-5p, hsa-miR-152-3p, hsa-miR-205-5p, hsa-miR-183-5p, and hsa-miR-487b-3p) co-regulate TP53 and Akt. mRNA expression levels of four genes co-targeted by two or more up-regulated miRNAs were significantly decreased after GDNF treatment (P < 0.05). Conclusion: GDNF treatment of U251 glioma cells significantly increased the expression of seven miRNAs involved in cell adhesion and the cell cycle.
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Zhang, Zhao, Bo Lei, Honggang Wu, Xiaoli Zhang, and Niandong Zheng. "Tumor suppressive role of miR-194-5p in glioblastoma multiforme." Molecular Medicine Reports 16, no. 6 (October 19, 2017): 9317–22. http://dx.doi.org/10.3892/mmr.2017.7826.
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Moreira-Costa, Liliana, António S. Barros, André P. Lourenço, Adelino F. Leite-Moreira, Rita Nogueira-Ferreira, Visith Thongboonkerd, and Rui Vitorino. "Exosome-Derived Mediators as Potential Biomarkers for Cardiovascular Diseases: A Network Approach." Proteomes 9, no. 1 (February 1, 2021): 8. http://dx.doi.org/10.3390/proteomes9010008.
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Cardiovascular diseases (CVDs) are widely recognized as the leading cause of mortality worldwide. Despite the advances in clinical management over the past decades, the underlying pathological mechanisms remain largely unknown. Exosomes have drawn the attention of researchers for their relevance in intercellular communication under both physiological and pathological conditions. These vesicles are suggested as complementary prospective biomarkers of CVDs; however, the role of exosomes in CVDs is still not fully elucidated. Here, we performed a literature search on exosomal biogenesis, characteristics, and functions, as well as the different available exosomal isolation techniques. Moreover, aiming to give new insights into the interaction between exosomes and CVDs, network analysis on the role of exosome-derived mediators in coronary artery disease (CAD) and heart failure (HF) was also performed to incorporate the different sources of information. The upregulated exosomal miRNAs miR-133a, miR-208a, miR-1, miR-499-5p, and miR-30a were described for the early diagnosis of acute myocardial infarction, while the exosome-derived miR-192, miR-194, miR-146a, and miR-92b-5p were considered as potential biomarkers for HF development. In CAD patients, upregulated exosomal proteins, including fibrinogen beta/gamma chain, inter-alpha-trypsin inhibitor heavy chain, and alpha-1 antichymotrypsin, were assessed as putative protein biomarkers. From downregulated proteins in CAD patients, albumin, clusterin, and vitamin D-binding protein were considered relevant to assess prognosis. The Vesiclepedia database included miR-133a of exosomal origin upregulated in patients with CAD and the exosomal miR-192, miR-194, and miR-146a upregulated in patients with HF. Additionally, Vesiclepedia included 5 upregulated and 13 downregulated exosomal proteins in patients in CAD. The non-included miRNAs and proteins have not yet been identified in exosomes and can be proposed for further research. This report highlights the need for further studies focusing on the identification and validation of miRNAs and proteins of exosomal origin as biomarkers of CAD and HF, which will enable, using exosomal biomarkers, the guiding of diagnosis/prognosis in CVDs.
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Khanizadeh, Sayyad, Mehrdad Ravanshad, Seyed Younes Hosseini, Parivash Davoodian, Mohammad Almasian, and Zahra Khanlari. "The effect of the hepatitis C virus (HCV) NS3 protein on the expression of miR-150, miR-199a, miR-335, miR-194 and miR-27a." Microbial Pathogenesis 110 (September 2017): 688–93. http://dx.doi.org/10.1016/j.micpath.2017.03.004.
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Senanayake, U., S. Das, P. Vesely, W. Alzoughbi, L. F. Frohlich, P. Chowdhury, I. Leuschner, G. Hoefler, and B. Guertl. "miR-192, miR-194, miR-215, miR-200c and miR-141 are downregulated and their common target ACVR2B is strongly expressed in renal childhood neoplasms." Carcinogenesis 33, no. 5 (March 19, 2012): 1014–21. http://dx.doi.org/10.1093/carcin/bgs126.
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Mencias, Mark, Michelle Levene, Kevin Blighe, and Bridget Bax. "Circulating miRNAs as Biomarkers for Mitochondrial Neuro-Gastrointestinal Encephalomyopathy." International Journal of Molecular Sciences 22, no. 7 (April 1, 2021): 3681. http://dx.doi.org/10.3390/ijms22073681.
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Mitochondrial neurogastrointestinal encephalomyopathy (MNGIE) is an ultra-rare disease for which there are currently no validated outcome measures for assessing therapeutic intervention efficacy. The aim of this study was to identify a plasma and/or serum microRNA (miRNA) biomarker panel for MNGIE. Sixty-five patients and 65 age and sex matched healthy controls were recruited and assigned to one of four study phases: (i) discovery for sample size determination; (ii) candidate screening; (iii) candidate validation; and (iv) verifying the performance of the validated miRNA panel in four patients treated with erythrocyte-encapsulated thymidine phosphorylase (EE-TP), an enzyme replacement under development for MNGIE. Quantitative PCR (qPCR) was used to profile miRNAs in serum and/or plasma samples collected for the discovery, validation and performance phases, and next generation sequencing (NGS) analysis was applied to serum samples assigned to the candidate screening phase. Forty-one differentially expressed candidate miRNAs were identified in the sera of patients (p < 0.05, log2 fold change > 1). The validation cohort revealed that of those, 27 miRNAs were upregulated in plasma and three miRNAs were upregulated in sera (p < 0.05). Through binary logistic regression analyses, five plasma miRNAs (miR-192-5p, miR-193a-5p, miR-194-5p, miR-215-5p and miR-34a-5p) and three serum miRNAs (miR-192-5p, miR-194-5p and miR-34a-5p) were shown to robustly distinguish MNGIE from healthy controls. Reduced longitudinal miRNA expression of miR-34a-5p was observed in all four patients treated with EE-TP and coincided with biochemical and clinical improvements. We recommend the inclusion of the plasma exploratory miRNA biomarker panel in future clinical trials of investigational therapies for MNGIE; it may have prognostic value for assessing clinical status.