Modulation of tamoxifen-induced apoptosis of ER-negative breast cancer cells by Bcl-2 and Caspase-3
- VernacularTitle:Bcl-2和Caspase-3调控他莫昔芬诱导的ER阴性乳腺癌细胞凋亡
- Author:
Dezong GAO
;
Jingzhong SUN
;
Yonggang LI
;
Lihua SHAO
;
Jintao LI
- Publication Type:Journal Article
- Keywords:
Breast Neoplasms/genet;
Apoptosis;
Bcl-2;
Caspase-3
- From:
Chinese Journal of General Surgery
2001;0(09):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the role of Bcl-2 and Caspase-3 in modulating apoptosis of ER-negative breast cancer cells induced by tamoxifen. Methods ER-negative breast cancer cell lines MDA-MB-231 were treated with 10.0?M tamoxifen for 12, 24, 36,48, 60 hours. The rate of cell apoptosis with or without caspase-3 inhibitor Ac-DEVD-CHO, and protein expression of Bcl-2,Bax were determined by flow cytometry, and the activity of Caspase-3 was examined with fluorophotometry. Results The expression of Bcl-2 was down-regulated, the activity of Caspase-3 and the rate of cell apoptosis were increased by TAM time-dependently, and the rate of apoptosis reached its peak at 48 hours. The expression of Bcl-2 was (negatively) correlated with activity of caspase-3. Tamoxifen, however, did not affect Bax protein expression. Ac-DEVD-CHO, a caspase-3 inhibitor, blocked the activation of caspase-3 and inhibited cell apoptosis (induced) by tamoxifen. Conclusions TAM could induce apoptosis in ER-negative breast cancer cells via (mitochondria) pathway by down-regulating Bcl-2 expression, and the activation of Caspase-3 might play an (important) role in the process of tamoxifen-induced apoptosis of ER-negative breast cancer cells.
