p16在重组人肿瘤坏死因子诱导的HepG2肝癌细胞凋亡中的作用研究

The effects of p16 in the apoptosis of HepG2 Hepatocellular carcinoma cells induced by recombinant mutant human tumor necrosis factor (rmhTNF)

目的:研究p16在重组人肿瘤坏死因子(rmhTNF)诱导的肝癌细胞凋亡中的作用。方法:用rmhTNF处理肝癌细胞,以流式细胞仪检测细胞周期变化,蛋白免疫印迹检测细胞内p16的表达变化。用siRNA干扰p16的表达后,再予流式细胞仪检测细胞的凋亡变化。结果:rmhTNF可以诱导肝癌细胞HepG2的凋亡,同时也可以诱导p16的表达的增加。干扰p16的表达可以逆转由rmhTNF诱导的肝癌细胞的凋亡。结论:p16在rmhTNF诱导的肝癌细胞的凋亡中发挥着重要的作用。

Objective： To investigate the effects of p16 in the apoptosis of HepG2 Hepatocellular carcinoma cells induced by recombinant mutant human tumor necrosis factor （rmhTNF）. Methods： HepG2 cells were treated with rmhTNF, cell cycle change was tested by flow eytometry, p16 expression was analyzed by western blot. The apoptosis of HepG2 cells was detected by flow cytometry after pretreatment of p16 with siRNA. Results： Treatment of rmhTNF to HepG2 Hepatocellular carcinoma ceils could induce cell apoptosis and the increased p16 expression. Knockdown p16 expression could reverse rmTNF-induced HepG2 cells apoptosis. Conclusion： p16 plays a critical role in the apoptosis of HepG2 hepatocellular carcinoma cell induced.by rmhTNF.