Journal
MOLECULAR MEDICINE REPORTS
Volume 12, Issue 5, Pages 6918-6924Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/mmr.2015.4254
Keywords
microRNA-122; mimic; apoptosis; HepG2 cell
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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.
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