Involvement of ERK signaling pathway in apoptosis of hepatic carcinoma induced by decitabine combined sodium valproate
10.3969/j.issn.1000-484X.2016.01.007
- VernacularTitle:地西他滨联合丙戊酸钠促进肝癌细胞凋亡的ERK通路研究
- Author:
Wufeng FAN
;
Hao LI
- Publication Type:Journal Article
- Keywords:
Decitabine;
Sodium valproate;
Hepatic carcinoma;
Apoptosis;
ERK signaling pathway
- From:
Chinese Journal of Immunology
2016;(1):33-36,41
- CountryChina
- Language:Chinese
-
Abstract:
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 MTT 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 ERK1/2 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.