Inhibition of MEK sensitizes human breast carcinoma cells to endoplasmic reticulum pathway's apoptosis
- VernacularTitle:抑制MEK对内质网应激诱导乳腺癌细胞凋亡的增敏作用
- Author:
Fen YANG
;
Hao LIU
;
Xudong ZHANG
;
Zhiwen JIANG
- Publication Type:Journal Article
- Keywords:
breast carcinoma;
ER stress;
GRP78;
Apoptosis;
MEK inhibition
- From:
Chinese Pharmacological Bulletin
1986;0(06):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the inhibition of MEK/ERK pathway affecting the sensitivity of human breast carcinoma cells SK-BR-3 to endoplasmic reticulum(ER) stress-induced apoptosis and wish to find new targets for human breast carcinoma chemotherapy.Methods Different concentrations(0,1.5,3,6,9 and 12 ?mol?L-1) tunicamycin(TM) treated human breast carcinoma cells SK-BR-3 for 48 h,then propidium iodide(PI) staining measured apoptotic cells in Flow Cytometry(FCM).Different times(0,6,12,24 and 36 h) of TM(3 ?mol?L-1) treated SK-BR-3 cells,Western blot measured proteins GRP78,ERK1/2 and pERK expression.MEK inhibitor U0126(20 ?mol?L-1) pretreated cells for 1 h before treatment with TM(3 ?mol?L-1) in different concentrations and times,measured above identical indexes and compared with their diversities of treatment with U0126 or not.Results TM induced apoptotic cells
