Mechanism of miR-107-targeting of regulator of G-protein signaling 4 in hepatocellular carcinoma.

Abstract

The aim of the present study was to investigate the mechanism of microRNA (miR)-107 in targeting regulator of G-protein signaling 4 (RGS4) in hepatic carcinoma. SK-HEP-1 cells were transfected with miR-107 mimics and control mimics. Reverse transcription-quantitative PCR was performed to determine the miR-107 expression levels, and following miR-107 upregulation, MTT, colony formation, transwell and wound-healing assays were performed to assess cell proliferation, colony-forming ability, invasion and migration, respectively. In addition, the effect of miR-107 upregulation on the cell cycle and apoptosis in SK-HEP-1 cells was evaluated using flow cytometry. Western blot analysis was performed to measure the protein expression levels of RGS4, epidermal growth factor receptor (EGFR), CXC chemokine receptor type 4 (CXCR4) and matrix metalloproteinase (MMP)-2 and −9. Expression level changes and the association between miR-107 and RGS4 in HCC cells were assessed using dual luciferase analysis. The results indicated that the overexpression of miR-107 in HCC cells suppressed cellular proliferation, invasion, migration and colony-forming ability, but promoted apoptosis and G1 phase arrest. Furthermore, miR-107 mimics notably increased the protein expression level of RGS4, but significantly downregulated that of EGFR, CXCR4 and MMP-2 and −9. Together, these findings suggest that targeting this potential mechanism of miR-107 may be beneficial in the treatment of patients with HCC.