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 distribution of endometrial cancer cells costimulated with 10(-6) mol/L E2 was detected by monotetrazolium (MTT) assay and fluorescence-activated cell sorting technique. RESULTS: With increased concentrations of E2, values of OD 570 nm for endometrial cancers increased gradually especially in Ishikawa. Cell cycle distribution analysis revealed that percentage of Ishikawa cells at G0-G1 phase decreased and percentage at S phase increased significantly, whereas that of HEC-1A cells did not 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, G0-G1 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 E2, make cells apoptosis and block Ishikawa cells at the G1/S transition. Therefore, ICI182780 may be a valid approach to treat ER-positive endometrial carcinoma.
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 distribution of endometrial cancer cells costimulated with 10(-6) mol/L E2 was detected by monotetrazolium (MTT) assay and fluorescence-activated cell sorting technique. RESULTS: With increased concentrations of E2, values of OD 570 nm for endometrial cancers increased gradually especially in Ishikawa. Cell cycle distribution analysis revealed that percentage of Ishikawa cells at G0-G1 phase decreased and percentage at S phase increased significantly, whereas that of HEC-1A cells did not 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, G0-G1 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 E2, make cells apoptosis and block Ishikawa cells at the G1/S transition. Therefore, ICI182780 may be a valid approach to treat ER-positive endometrial carcinoma.