Effect of 17β-E_2 on proliferation and expression of p-Erk in endometrial carcinoma cells
Guo Ruixia
Abstract
Guo Ruixia
Abstract
Objective To observe the influence of 17 β-estradiol(E2) on proliferation,cell cycle progression,expressions of p-Erk in endometrial carcinoma cells Ishikawa and HEC-1A.Methods 17β-E2 was used to Ishikawa and HEC-1A cells,the proliferation and cell cycle of Ishikawa and HEC-1A were detection by MTT and fluorescence-activated cell sorting technique,the p-Erk were examined by immunoprecipitation in Ishikawa and HEC-1A cell after stimulated with 10-6 mol/L 17β-E2 for different times.Results With increased concentrations of 17β-E2,the proliferation of Ishikawa cell increased gradually and in a time-dependent manner(P0.01),percentage of Ishikawa cell at G0~G1 phase decreased(P0.01)and percentage of S phase cells increased significantly(P0.01),whereas that of HEC-1A cell didn′t show significant alteration.The maximal activation of p-Erk took place at 30 min in Ishikawa cell and 15 min in HEC-1A cell after stimulation with 10-6 mol/L 17β-E2.Conclusion 17β-E2 not only promote the cell proliferation and the cell cycle distrubion of endometrial carcinoma cell lines,but also activate promptly MAPK signaling pathway by non-nuclear actions in endometrial carcinoma cells.
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Objective To observe the influence of 17 β-estradiol(E2) on proliferation,cell cycle progression,expressions of p-Erk in endometrial carcinoma cells Ishikawa and HEC-1A.Methods 17β-E2 was used to Ishikawa and HEC-1A cells,the proliferation and cell cycle of Ishikawa and HEC-1A were detection by MTT and fluorescence-activated cell sorting technique,the p-Erk were examined by immunoprecipitation in Ishikawa and HEC-1A cell after stimulated with 10-6 mol/L 17β-E2 for different times.Results With increased concentrations of 17β-E2,the proliferation of Ishikawa cell increased gradually and in a time-dependent manner(P0.01),percentage of Ishikawa cell at G0~G1 phase decreased(P0.01)and percentage of S phase cells increased significantly(P0.01),whereas that of HEC-1A cell didn′t show significant alteration.The maximal activation of p-Erk took place at 30 min in Ishikawa cell and 15 min in HEC-1A cell after stimulation with 10-6 mol/L 17β-E2.Conclusion 17β-E2 not only promote the cell proliferation and the cell cycle distrubion of endometrial carcinoma cell lines,but also activate promptly MAPK signaling pathway by non-nuclear actions in endometrial carcinoma cells.
Key concepts: Cell growth, MAPK/ERK pathway, Cell cycle, Cell, Chemistry, Cell sorting, Cell biology, Carcinoma