Effects of ICI182780 (Faslodex) on proliferation and apoptosis induced by 17?-estradiol in endometrial carcinoma cells
- VernacularTitle:雌激素受体拮抗剂ICI182780(Faslodex)对17?-雌二醇作用下子宫内膜癌细胞增殖和凋亡的影响
- Author:
Rixia GUO
;
Lihui WEI
;
Dan ZHAO
;
Jianliu WANG
;
Xiaoping LI
- Publication Type:Journal Article
- Keywords:
Endometrial neoplasms;
Receptors, estrogen;
Estradiol;
Apoptosis;
Cell cycle
- From:
Journal of Peking University(Health Sciences)
2003;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To observe the influence of estrogen receptor, ICI182780, on proleferation, cell cycle progression and apoptosis in estrogen receptor (ER)-positive and ER-poor endometrial carcinoma cells and to explore the possible preliminary value of ICI182780 treating endometrial carcinoma. Methods: The effects of ICI182780 on proliferation, apoptosis and cell cycle distrubution of endometrial cancer cells costimulated with 10~ -6 of mol/L E_2 was detected by monotetrazolium (MTT) assay and fluorescence-activated cell sorting technique. Results: With increased concentrations of E_2, values of OD 570 nm for endometrial cancers increased gradually especially in Ishikawa. Cell cycle distribution analysis revealed that percentage of Ishikawa cells at G_0-G_1 phase decreased and percentage at S phase increased significantly, whereas that of HEC-1A cells didn’t show significant alteration. In cotreatment of endometrial cancer cells with ICI182780, values of OD 570 nm and numbers of apoptotic cells of Ishikawa cells decreased to basal levels, G_0-G_1 phase proportion increased, percentage of S phase increased in a time- or time-dependent manner. But there was no such alteration in HEC-1A cells. Conclusion: The specific ER antagonist, ICI182780, can inhibit Ishikawa cell propagation induced by E_2, make cells apoptosis and block Ishikawa cells at the G_1/S transition. Therefore, ICI182780 may be a valid approach to treat ER-positive endometrial carcinoma.
