摘要
目的研究细胞有丝分裂前期检查点(checkpoint with forkhead associated and ring finger,CHFR)在人肝癌细胞株HepG2中的表达,以及CHFR基因甲基化对HepG2细胞凋亡作用的影响。方法采用去甲基化剂5-氮-2-脱氧胞苷(5-Aza-2-deoxycytidine,Aza)处理人肝癌细胞株HepG2,半定量RT-PCR和Western-Blot检测CHFR在HepG2细胞中的表达水平,FCM分析HepG2细胞的凋亡情况。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,肿瘤细胞凋亡率逐渐增高,存在剂量-反应关系;且CHFR表达水平与HepG2细胞凋亡率呈正相关。结论在本试验条件下,CHFR在HepG2细胞中表达缺失,去甲基化后表达恢复;CHFR的高表达可以促进肝癌细胞凋亡。
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 apoptosis. 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 and Western Blot. The apoptosis of HepG2 cells was analyzed by flow cytometry. Results CHFR was not expressed in HepG2 cells. CHFR was recovered to express after the treatment of Aza. The apoptosis ratio of HepG2 cells increased. They showed dose-effect relationship. The expression level of CHFR was positively correlated with the apoptosis ratio of HepG2 cells. Conclusion In this experimental condition,CHFR was loss of expression in HepG2 cells and recovered by the methylation inhibition. CHFR hyperexpression may promote the apoptosis of hepatoma carcinoma cells.
出处
《毒理学杂志》
CAS
CSCD
北大核心
2010年第3期199-202,共4页
Journal of Toxicology
