Huang Hongyan, Zhu Yueyong, Li Shaoyang
Liver Diseases Research Center, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian 350005, P.R. China.
Department of Neurosurgery, The First People's Hospital of Taizhou, Taizhou, Zhejiang 318000, P.R. China.
Mol Med Rep. 2015 Nov;12(5):6918-24. doi: 10.3892/mmr.2015.4254. Epub 2015 Aug 26.
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.
目前对人类肝细胞癌（HCC）有效的治疗策略存在需求，HCC是癌症相关死亡的主要原因。微小RNA - 122（miR - 122）是内源性凋亡调节因子Bcl - w的抑制剂，在HCC中经常下调。因此，推测在HCC模型中，miR - 122的激活可能通过半胱天冬酶激活诱导选择性肝细胞凋亡。在本研究中，对HepG2细胞进行了miR - 122模拟物转染，并用于研究miR - 122在调节HCC衍生细胞系中的作用和治疗潜力。miR - 122模拟物转染后，HepG2细胞的凋亡率显著增加。逆转录-聚合酶链反应分析显示，Bcl - w mRNA显著降低，而半胱天冬酶-9和半胱天冬酶-3的mRNA水平显著增加。免疫细胞化学结果支持mRNA趋势。总体而言，本研究结果表明内源性miR - 122促进HepG2细胞凋亡，并且模拟miR - 122转染可使HCC模型中的凋亡水平正常化。
