miR-195 inhibits esophageal cancer cell proliferation and promotes apoptosis by downregulating YAP1

miR-195通过下调YAP1抑制食管癌细胞增殖并促进细胞凋亡

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作者:Xinyue Gao, Mingjun Lu, Weijuan Xu, Centao Liu, Jianping Wu

Conclusion

Decreased expression of miR-195 plays a regulatory role in increasing YAP1 expression and promoting the pathogenesis of esophageal cancer. Elevation of miR-195 inhibites the expression of YAP1, restrains cell proliferation, and promotes cell apoptosis.

Methods

The tumor tissue and the adjacent tissue of patients with esophageal cancer were collected to detect the expressions of miR-195 and YAP1. Dual luciferase reporter gene assay was adopted to validate the targeted regulation between miR-195 and YAP1. Esophageal cancer EC9706 cells and normal esophageal epithelial HEEC cells were cultured in vitro to measure the expression of miR-195 and YAP1. EC9706 cells were divided into miR-NC group and miR-195 mimic group followed by analysis of cell apoptosis by flow cytometry and cell proliferation by EdU staining.

Objective

Yes-associated protein 1 (YAP1) regulates a variety of genes related to cell proliferation, cycle and apoptosis, and plays a role in the pathogenesis of esophageal cancer. It was found that the expression of miR-195 was significantly decreased in esophageal cancer tissues, suggesting its anti-cancer effect. Bioinformatics analysis revealed the targeted relationship between miR-195 and the 3'-UTR of YAP1. This study investigated the role of miR-195 in regulating YAP1 expression and affecting proliferation and apoptosis of esophageal cancer cells.

Results

Compared with adjacent tissues, miR-195 was significantly decreased, while YAP1 mRNA and protein were significantly upregulated in esophageal cancer tissues. Dual luciferase reporter gene assay confirmed that there was a targeted relationship between miR-195 and YAP1. Compared with HEEC cells, miR-195 expression was declined, whereas YAP1 was elevated in EC9706 cells. Transfection of miR-195 mimic significantly downregulated YAP1 expression, resulting in increased apoptosis and decreased proliferation of EC9706 cells.

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