中国比较医学杂志2017，Vol.27Issue(12)：56-60,5.DOI:10.3969.j.issn.1671-7856.2017.12.010
罗格列酮对HT29、HCT116结肠癌细胞凋亡影响及机制探究
Rosiglitazone promotes apoptosis in colon cancer HT29 and HCT116cells through AKT/GSK3βsignalling pathway
摘要
Abstract
Objective To investigate the effect of rosiglitazone on the proliferation and apoptosis of colon cancer cells and the changes in the AKT/GSK3β signaling pathway. Methods Different concentrations of rosiglitazone ( 20. 0μmol/L, 40. 0 μmol/L, 80. 0 μmol/L) were used to treat colon cancer HT29 cells and HCT116 cells. Cell proliferation was detected by MTT assay. Annexin V FITC/PI cell death detection kit was used to test the cell apoptosis rate. The expression of apoptotic protein Bcl-2, Bax and Akt, GSK3β were detected by Western blot. Results Different concentrations of rosiglitazone had different effect on the proliferation of colon cancer cells compared with the blank control group, and showed a dose dependence (P< 0. 01). With the increase of rosiglitazone dose, the apoptosis-inducing effect @was increased dose-dependently (P< 0. 01). When the cells were treated with rosiglitazone for 48 h, the expressions of Bcl-2/Bax, p-GSK3β, and p-Akt were significantly decreased compared with the blank control group (P< 0. 01), but the expression level of Akt and GSK3β was not significantly different compared with the blank control group ( P > 0. 05 ) . Conclusions Rosiglitazone significantly induces apoptosis and inhibits the proliferation of HT29 cells. It may be via inhibiting Akt/GSK3β signaling pathway and change the ratio of Bcl-2/Bax.关键词
罗格列酮/结肠癌/凋亡/Bcl2/Bax/Akt/GSK3βKey words
Rosiglitazone/Colon cancer/Apoptosis/Bcl-2/Bax/Akt/GSK3β分类
医药卫生引用本文复制引用
张琪,杨光华,葛志鹏,丁家杉,黄志强,郑阳,张国志,王长友..罗格列酮对HT29、HCT116结肠癌细胞凋亡影响及机制探究[J].中国比较医学杂志,2017,27(12):56-60,5.基金项目
2017年政府资助省级临床医学优秀人才项目 （）
中国煤炭工业协会2017 年度科学技术研究指导性计划项目( MTKJ2017 -331). （ MTKJ2017 -331）
