MiR-125a-5p inhibits EMT of ovarian cancer cells by regulating TAZ/EGFR signaling pathway.

Abstract

To investigate the influences of micro ribonucleic acid (miR)-125a-5p on epithelial-mesenchymal transition (EMT) of ovarian cancer cells by regulating the transcriptional co-activator with PDZ-binding motif (TAZ)/epidermal growth factor receptor (EGFR) signaling pathway. The human ovarian cancer cells were cultured, and miR-125a-5p was repressed by inhibitor and overexpressed by miRNA mimics. The expression of EMT-related proteins was measured via Western blotting (WB). The action target of miR-125a-5p was determined through a dual-luciferase reporter gene assay. The changes in protein levels were detected via WB. MiR-125a-5p was down-regulated remarkably in ovarian cancer tissues. The expression level of serum miR-125a-5p in patients with ovarian cancer was lower than that in control group. After inhibition on miR-125a-5p, the expression level of E-cadherin, an epithelial indicator, was decreased, while that of Vimentin, an interstitial indicator, was increased. MiR-125a-5p contained a complementary site in the 3'-untranslated region (UTR) of TAZ messenger RNA (mRNA). The expressions of TAZ mRNA and protein in cells were down-regulated markedly after the overexpression of miR-125a-5p. The expressions of EGFR, phosphorylated EGFR (p-EGFR) and p-Akt were up-regulated in the cells transfected with miR-125a-5p mimics and those transfected with miR-125a-5p mimics overexpressing TAZ. MiR-125a-5p can inhibit the EMT of ovarian cancer cells by regulating the TAZ/EGFR signaling pathway.