MicroRNA-466 inhibits cancer cell migration and invasion in hepatocellular carcinoma by indirectly mediating the downregulation of ROCK2.

Abstract

MicroRNA-466 was recently characterized as a tumor suppressor with known biological function in prostate cancer. The aim of the current study was to investigate the possible involvement of microRNA-466 in hepatocellular carcinoma (HCC). The current study demonstrated that the expression level of microRNA-466 was significantly downregulated; while the mRNA expression level of Rho-associated coiled-coil containing protein kinase 2 (ROCK2) was significantly upregulated in tumor tissue compared with adjacent healthy tissue samples obtained from patients with HCC. In addition, the relative plasma level of microRNA-466 was significantly decreased, while the relative plasma level of ROCK2 was significantly increased in patients with HCC compared with healthy controls. Expression levels of microRNA-466 and ROCK2 were inversely correlated in tumor tissue but not in adjacent healthy tissue samples obtained from patients with HCC. Plasma levels of microRNA-466 and ROCK2 were inversely correlated in patients with HCC but not in healthy controls. In addition, reduced plasma levels of microRNA-466 may have a diagnostic value in the detection of early stage HCC. MicroRNA-466 overexpression significantly suppressed ROCK2 expression in HCC cells, whereas ROCK2 overexpression did not significantly affect microRNA-466 expression. MicroRNA-466 overexpression significantly suppressed, while ROCK2 overexpression significantly enhanced HCC cell migration and invasion. In addition, ROCK2 overexpression partially reversed the inhibitory effect of microRNA-466 overexpression on HCC cell migration and invasion. Taken together, these results suggest that microRNA-466 may inhibit HCC cell migration and invasion by indirectly mediating the downregulation of ROCK2.