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作 者:韩毓[1] 姜声扬[1] 王海健[1] 陈玉均[1]
机构地区:[1]南通大学公共卫生学院职业医学与环境毒理学教研室,江苏226007
出 处:《交通医学》2009年第3期248-251,共4页Medical Journal of Communications
摘 要:目的:研究CHFR基因在人肝癌细胞株HepG2中的表达,以及CHFR基因甲基化对HepG2细胞生长与集落形成的影响。方法:采用去甲基化剂5-氮-2-脱氧胞苷处理人肝癌细胞株HepG2,半定量RT-PCR检测CHFR在HepG2细胞中的表达变化,CCK法和平板集落形成试验分析HepG2细胞生长增殖情况的改变。结果:CHFR在HepG2细胞中表达缺失;经Aza去甲基化处理后,CHFR在HepG2细胞中逐渐恢复表达,肿瘤细胞抑制率和集落形成抑制率都逐渐增高,均存在剂量-反应关系;且CHFR表达水平与HepG2细胞抑制率、集落形成抑制率均呈正相关。结论:CHFR对于肝癌细胞的生长增殖能力发挥负向调控作用。Objective: To study the expression of CHFR (checkpoint with forkhead associated and ring finger) in human hepatoma carcinoma cell line HepG2 and the effect of CHFR DNA methylation on the HepG2 cells growth and colony formation. Methods: Human hepatoma carcinoma cell line HepG2 was treated by methylation inhibitor 5-Aza-2-deoxycytidine (Aza). The expression level of CHFR in HepG2 cells was evaluated by semi-quantitative RT-PCR. The cell growth and proliferation of HepG2 ceils was analyzed by CCK assay and colony formation test. Results: CHFR was not expressed in HepG2 cells. CHFR was recovered to express after the treatment of Aza. The inhibition ratio of both HepG2 cells proliferation and colony formation increased. They showed dose-effect relationship. The expression level of CHFR was positively correlated with the inhibition ratio of HepG2 cells proliferation and colony formation. Conclusion: CHFR was not expressed in HepG2 cells and recovered by the methylation inhibition. CHFR may play a negative role during the growth and proliferation of hepatoma carcinoma cells..
关 键 词:CHFR基因 HEPG2细胞 5-氮-2-脱氧胞苷 DNA甲基化
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