Effects of 17β-estradiol on proliferation and expressions of P21ras and p-Erk in Ishikawa cells

Aim:To observe the influence of 17β-estradiol on proliferation,cell cycle progression,expressions of P21ras and p-Erk in endometrial carcinoma Ishikawa cells and to explore the possibility of endometrial carcinoma induced by estradiol.Methods:The effects of estradiol on proliferation,cell cycle phase of endometrial carcinoma Ishikawa cells were detected using MTT assay and fluorescence-activated cell sorting technique.The activity of P21ras and p-Erk were examined by immunoprecipitation in Ishikawa cells after stimulation with 10-6 mol/L E2 for different times(0,5,15,30 min,and 1,2 h) to observe the optimal time and with varied doses of E2(0,10-10,10-8,10-6,10-4 mol/L)for the optimal time.Results:With increased concentrations of E2,the proliferation of Ishikawa cells increased in a time-dependent manner(P0.05). Cell cycle phase analysis revealed that percentage of Ishikawa cells at G0-G1 phase (P0.05) decreased and percentage of S phase cells increased significantly(P0.05).The maximal activation of P21ras and p-Erk took place at 30 min in Ishikawa cells [(74.00±2.54)%,(68.00±4.81)%] after stimulation with 10-6 mol/L E2(P0.05).With increased doses of E2,the expression of P21ras and p-Erk increased in a concentration-dependent manner(P0.05). Between the expressions of P21ras and p-Erk,there was significant positive correlationship(P0.05).Conclusion:17β-estradiol not only could promote the cell proliferation and the cell cycle progression of endometrial carcinoma Ishikawa cells,but also activate promptly MAPK signaling pathway by non-nuclear actions in endometrial carcinoma cells.