Effects and mechanisms of microRNA-122 on invasion and migration of hepatocellular carcinoma cells

Abstract

Objective To detect the expression of miR-122 in hepatocellular carcinoma (HCC) cells and tissues, and to explore the role and the underlying mechanisms of miR-122 in HCC cells on invasion and migration. Methods Real-time quantitative polymerase chain reaction of analysis was used to examine the expression of miR-132 in HCC cell lines, a normal liver cell line, HCC tissues and adjacent non-tumor tissues. Over express or inhibit miR-122 by transfection. The invasion and migration of HCC cells were analyzed by Transwell assays. Meanwhile, related mechanism proteins were detected by western blot, including insulin like growth factor 1 receptor(IGF-1R), E-cadherin, vimentin. Results The expression of miR-122 was decreased in HCC tissue samples compared with the adjacent non-tumor tissues[(20.5±4.2)×10-4 vs. (30.3±5.6)×10-4], especially in HCC tissue samples with HBV[(25.6±3.5)×10-4 vs. (19.1±3.2)×10-4]. The same results were observed in HCC cell lines. MHCC-97H cells exhibited lowest level of miR-122 expression[(33.7±1.3)×10-3], whereas SMMC-7721 exhibited the highest level of miR-122 expression [(65.3±1.3)×10-3]. MiR-122 over-expression suppressed the invasion and migration of MHCC-97H[(218.7±24.0) vs. (418.0±23.4), (392.7±12.8) vs. (706.6±19.8)]. Knocking down miR-122 promoted the invasion and migration of SMMC-7721[(233.0±14.4) vs. (145.0±8.0), (561.3±9.6) vs. (218.0±11.3)]. Western blot revealed that miR-122 suppressed the expression of IGF-1R, Vimentin and facilitated the expression of E-cadherin. Conclusions The study indicates that miR-122 is downregulated in HCC, especially in HCC tissue samples with HBV. MiR-122 can suppress invasion and migration of hepatocellular carcinoma by regulating IGF-1R and epithelial mesenchymal transition, and may provide a new therapeutic option for HCC. Key words: MicroRNA-122; Hepatocellular carcinoma; Insulin like growth factor 1 receptor; Epithelial mesenchymal transition; Tumor invasion