实用肿瘤学杂志 ›› 2012, Vol. 26 ›› Issue (5): 428-431.doi: 10.3969/j.issn.1002-3070.2012.05.010

• 论著 • 上一篇    下一篇

MiR-122促进原发性肝细胞癌Huh-7细胞凋亡

栾天1, 佟雷2, 徐威2, 钟照华2   

  1. 1.哈尔滨医科大学肿瘤防治研究所(哈尔滨 150081);
    2.哈尔滨医科大学微生物教研室
  • 收稿日期:2012-06-21 出版日期:2012-05-25 发布日期:2012-10-29
  • 通讯作者: 钟照华,E-mail:zhonghmu@gmail.com
  • 作者简介:栾天,女,(1982-),硕士,研究实习员,从事肿瘤基础研究

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

LUAN Tian1,TONG Lei2,XU Wei2,ZHONG Zhaohua2   

  1. 1.Cancer Research Institute,Harbin Medical University,Harbin 150081,China;
    2.Department of Microbiology,Harbin Medical University
  • Received:2012-06-21 Online:2012-05-25 Published:2012-10-29

摘要: 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24 h、48 h用流式细胞法、TUNEL法检测细胞凋亡及细胞周期。结果 转染后24 h、48 h,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48 h,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24 h、48 h,转染miR-122、Mock的HepG2细胞,各细胞周期组份均无统计学意义(P>0.05),但于转染后48 h,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。

Abstract: 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 deoxynucleotidy1 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 G0~G1 phase was significantly up-regulated,compared with that of mock cells.The rates in S phase and G2-M phase were down-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.

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