MiRNA-206 inhibits hepatocellular carcinoma cell proliferation and migration but promotes apoptosis by modulating cMET expression.

Abstract

A close relationship between cancer progression and microRNAs (miRNAs) regulation has been demonstrated. Abnormal microRNA-206 (miR-206) expression has been shown to be related to the development of malignancies. However, the role of miR-206 in hepatocellular carcinoma (HCC) remains unclear. Here, we evaluated the function of miR-206 in HCC. Results showed that miR-206 expression was decreased in 27 human HCC tissues compared with that of adjacent normal tissues. Conversely, cMET was up-regulated in human HCC cancer tissues, and cMET levels were shown to be negatively correlated with miR-206 expression. Abnormally increased miR-206 expression in three HCC cell lines (SMMC-7721, HepG2, and Huh7) attenuated cell viability, migration, and invasion. Increased apoptosis was also observed in these miR-206 expressing cells. Furthermore, we identified that miR-206 targets the 3'-UTR of the cMET gene for silencing, and restoration of cMET expression reversed the inhibitory effect of miR-206 on HCC. Tumor cells expressing miR-206 also showed delayed growth in the in vivo experiments compared with the controls. Altogether, our findings provide new insights into the molecular mechanisms of HCC oncogenesis.