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Mol Med Rep. 2015 Nov;12(5):6918-24. doi: 10.3892/mmr.2015.4254. Epub 2015 Aug 26.

MicroRNA-122 mimic transfection contributes to apoptosis in HepG2 cells.

Author information

1
Liver Diseases Research Center, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350005, P.R. China.
2
Department of Neurosurgery, The First People's Hospital of Taizhou, Taizhou, Zhejiang 318000, P.R. China.

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.

PMID:
26323254
DOI:
10.3892/mmr.2015.4254
[Indexed for MEDLINE]

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