TSA-induced apoptosis of gastric carcinoma SGC-7901 cell and its mechanism
- VernacularTitle:组蛋白去乙酰化酶抑制剂诱导人胃癌细胞SGC-7901凋亡及其机制
- Author:
Yazhou LI
;
Weidong GONG
;
Rui ZHAN
;
Daihui NI
;
Wenxian LI
;
Zhimin WANG
;
Zhiqun WU
- Publication Type:Journal Article
- Keywords:
gastric carcinoma;
histone deacetylase inhibitor;
tumor therapy;
carcinogenesis;
apoptosis
- From:
Journal of Interventional Radiology
2010;19(3):220-223
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the apoptosis of gastric carcinoma SGC-7901 cell induced by histone deacetylase inhibitor(TSA)and to clarify its mechanisms.Methods The apoptosis-inducing role of TSA on gastric carcinoma SGC-7901 cell was investigated with the help of cell proliferation assay,Annexin V stain,cell flow analyzer and Tunel assay.Western blot,gene chips,real time PCR were employed to study the influence and mechanisms of TSA on the expression of gastric carcinoma cell SGC-7901 p53,bax,etc.Results TSA could induce the apoptosis of gastric carcinoma SGC-7901 cells,increase the expression of p53 and bax,and decrease the expression of bcl-2.survivin and easpase in gastric carcinoma SGC-7901 cells.TSA could transfer AIF and EndoG from mitochondria to nucleus.The apoptosis induced by TSA was brought about through the regulation of multiple apoptosis-related genes,and the apoptosis pathway induced by TSA was caspase-independent.Conclusion TSA can induce caspase-independent apoptosis in gastric carcinoma SGC-7901 cell through the regulation of multiple apoptosis-related genes.