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

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 prevented cell migration and invasion, and induced the enhancement of E-cadherin expression and the decreased levels of N-cadherin, Vimentin and Snail as well as expressions of SOX2, OCT4 and Bmi1, restraining metastasis and stemness of HCC in vitro. Mechanistically, miR-3682-3p was positively activated by c-Myc, and could directly target PTEN to activate PI3K/AKT pathway. In addition, inhibition of PTEN weakened the anti-metastatic and anti-stemness effects of miR-3682-3p downregulation in HCC cells. Conclusion: From these findings, we concluded that miR-3682-3p promoted HCC metastasis and stemness through PTEN/PI3K/AKT signaling, implying that miR-3682-3p might be a promising target for HCC clinical treatment.