MicroRNA-122 mimic transfection contributes to apoptosis in HepG2 cells

Abstract

There is currently a requirement for effective treatment strategies for human hepatocellular carcinoma (HCC), a leading cause of cancer-associated mortality. MicroRNA-122 (miR-122), a repressor of the endogenous apoptosis regulator Bcl-w, is frequently downregulated in HCC. Thus, it is hypothesized that the activation of miR-122 may induce selective hepatocellular apoptosis via caspase activation in a model of HCC. In the present study, an miR-122 mimic transfection was performed in HepG2 cells, and used to investigate the role and therapeutic potential of miR-122 in the regulation of HCC-derived cell lines. The apoptotic rates of HepG2 cells were significantly increased following miR-122 mimic transfection. Reverse transcription-polymerase chain reaction analysis revealed that Bcl-w mRNA was significantly reduced, while the mRNA levels of caspase-9 and caspase-3 were markedly increased. The immunocytochemistry results supported the mRNA trends. Collectively, the present results suggest that endogenous miR-122 contributes to HepG2 apoptosis and that transfection of mimic miR-122 normalizes apoptotic levels in a model of HCC.