MiR-122促进原发性肝细胞癌Huh-7细胞凋亡

MiR- 122 stimulates the apoptosis of hepatoma cell Huh- 7

目的探讨miR-122对原发性肝细胞癌（hepatocellular carcinoma，HCC）细胞性状的影响。方法HepG2细胞、Huh-7细胞分别转染miR-122、anti—miR-122，转染Mock组作为阴性对照，分别于转染后24h、48h用流式细胞法、TUNEL法检测细胞凋亡及细胞周期。结果转染后24h、48h，转染miR-122、Mock的HepG2细胞两组间细胞凋亡率均无统计学意义（P〉0．05），而在转染后48h，与Mock组Huh-7细胞相比，转染anti—miR-122的Huh-7细胞凋亡率明显降低（P〈0．05）；转染后24h、48h，转染miR-122、Mock的HepG：细胞，各细胞周期组份均无统计学意义（P〉0．05），但于转染后48h，转染anti—miR-122的Huh-7细胞可见G0-G1期细胞明显多于Mock组，S期、G2-M期细胞则显著少于Mock组（P〈0．05）。结论miR-122表达水平的下降能够抑制某些HCC细胞如Huh7细胞凋亡，miR-122可能作为一种内源性凋亡调控因子，在肝脏组织中发挥抗肿瘤作用。

Objective To identify the effects of miR - 122 （a hepatic microRNA）on the cellular behavior of hepatocellular carcinoma cells （HCC）. Methods The apoptosis and cell cycle of HepG2 and Huh - 7 cells transfected with miR - 122 or anti - miR - 122 were analyzed by Annexin V - based flow cytometry,terminal deoxynucleotidyl transferase dUTP nick end labeling（TUNEL）detection as well as PI- based flow cytometry at 24 and 48 h posttransfection. Cells transfected with Mock were served as negative controls. Results There was no significant difference between the apoptosis, cell cycles of HepG2 cells transfected with miR -122 and Mock HepG2 cells at 24,48 h posttransfection（ P 〉 0.05 ）. However, compared to Mock Huh - 7 cells, the apoptosis of Huh - 7 cells transfected with anti - miR - 122 was signaficantly decreased at 48 h posttransfection（ P 〈 0.05 ） ; the rate of Huh -7 cells treated with anti - miR - 122 in GO - G1 phase was significantly up - regulated, compared with that of mock cells. The rates in S phase and G2 -M phase were clown -regulated（ P 〈 0.05 ）. Conclusion The down - regulation of miR - 122 expression might prevent the apoptosis of certain type of HCC, such as Huh -7 cells, miR - 122 may be as an endogenous regulating factor of apoptosis to play the antineoplastic effect in the liver tissues.