摘要
目的:本研究对地西他滨联合丙戊酸钠促进肝癌细胞凋亡的相关机制进行研究,为临床治疗和新药研发提供参考。方法:肝癌细胞HepG2经地西他滨联合丙戊酸钠孵育后,MTT法检测二者对HepG2细胞的抑制率,Real-time PCR及免疫印迹法检测细胞凋亡蛋白Caspase3/9、Bax及Bcl2和ERK信号通路关键蛋白的表达情况。结果:地西他滨联合丙戊酸钠能够有效抑制肝癌细胞的增殖,且二者联用的抑制率明显高于单独应用(P<0.05),同时与对照组相比,细胞凋亡蛋白Caspase3、Caspase9及Bax表达明显增强(P<0.05),Bcl2表达明显降低(P<0.05),且ERK信号通路关键蛋白Ras、Raf及MEK和ERK1/2的表达明显升高,与对照组细胞有显著的统计学差异性(P<0.05)。结论:地西他滨联合丙戊酸钠主要通过激活MEK/ERK信号转导通路抑制肝癌细胞HepG2的增殖过程。
Objective：The present research aimed to explore the involvement of ERK signaling pathway in apoptosis of hepatic carcinoma induced by decitabine combined sodium valproate. Methods： HepG2 cell line was incubated with decitabine combined sodium valproate and the inhibition rate was detected by MTF method. The apoptotic related protein and ERK signal pathway proteins were assayed by Real-time PCR or Western blot. Results： The HepG2 cell line was inhibited greatly by decitabine combined sodium valproate medication with an increased expression of Caspase3, Caspase9 and Bax （ P〈0.05 ）. The expression of Ras, Raf, MEK and ERKI/2 was increased dramatically after incubation with decitabine combined sodium valproate when compared with control group （ P〈 0. 05 ）. Conclusion： Decitabine combined sodium valproate exert a significant inhibition on the proliferation of HepG2 cell line by nor- malizing the abnormal MEK/ERK signaling pathway.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2016年第1期33-36,41,共5页
Chinese Journal of Immunology
关键词
地西他滨
丙戊酸钠
肝癌
细胞凋亡
ERK信号通路
Decitabine
Sodium valproate
Hepatic carcinoma
Apoptosis
ERK signaling pathway
