miR-3682-3p activated by c-Myc aggravates the migration and stemness in hepatocellular carcinoma cells by regulating PTEN/PI3K/AKT/β-catenin signaling

Abstract

Objective: To elusive the underlying mechanism and functions of miR-3682-3p in hepatocellular carcinoma (HCC). Methods: Thirty pairs of tumor tissues and adjacent tissues were obtained from HCC patients. mRNA and protein expressions were detected by quantitative real-time PCR and western blot, respectively. The migration and invasion were measured using transwell or wound healing assays. Dual luciferase and ChIP assays were utilized to detect gene interactions. Results: miR-3682-3p was highly expressed in HCC tissues and cell lines. Silencing of miR-3682-3p inhibited cell migration and invasion, increased E-cadherin expression, and decreased N-cadherin, Vimentin and Snail expressions, as well as the of SOX2, OCT4 and Bmi1 expression, thereby restraining EMT and stemness of HCC in vitro. miR-3682-3p was positively activated by c-Myc, and could directly target PTEN to activate PI3K/AKT/β-catenin pathway. In addition, inhibition of PTEN weakened the anti-migration and anti-stemnesic effects of miR-3682-3p downregulation in HCC cells. Conclusion: miR-3682-3p promoted HCC migration and stemness through PTEN/PI3K/AKT/β-catenin signaling, implying that miR-3682-3p might be a promising target for HCC clinical treatment.