摘要
目的:探讨YM155对肝癌HepG2细胞增殖和凋亡的影响及可能的机制。方法:采用CCK-8法检测细胞生长抑制率;应用流式细胞仪检测细胞凋亡率的变化;Western blot法检测细胞中蛋白表达的变化,实时定量RT-PCR检测survivin mRNA表达的变化。结果:YM155对人肝癌HepG2细胞的生长抑制作用呈现剂量和时间依赖性。流式细胞术结果显示,HepG2细胞凋亡率明显升高,呈现剂量依赖性。YM155可引起survivin mRNA及蛋白表达下降,而caspase-3、caspase-9和PARP蛋白表达上升。结论:YM155可以抑制人肝癌HepG2细胞的增殖并促进其凋亡,其机制可能是通过激活caspase凋亡途径来实现。
Objective:To investigate the effects of YM155 on human hepatic carcinoma cell lines HepG2 and the possible mechanisms.Methods:Cell growth inhibition rates were determined by CCK-8 assay.The apoptosis rates of HepG2 cells were analyzed by flow cytometry.The expression levels of proteins were detected by Western blot.Survivin mRNA expression was determined by real time polymerase chain reaction(RT-PCR).Results:The proliferation rate of HepG2 cells in the YM155 treated group decreased in a dose-and-time-dependent manner.FCM results showed that the apoptosis rate of HepG2 cells was increased in a dose-dependent manner.YM155 could significantly down-regulate mRNA and protein levels of survivin.It can also up-regulate caspase-3,caspase-9 and PARP protein levels.Conclusion:YM155 can inhibit proliferation and induce apoptosis of HepG2 cells through activating the apototic signal pathway of caspase.
作者
时汀
张建淮
Shi Ting;Zhang Jianhuai(The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University,Jiangsu Huaian 223300,China)
出处
《现代肿瘤医学》
CAS
2019年第14期2473-2476,共4页
Journal of Modern Oncology