Effect of Estrogen on Growth of Estrogen Receptor Negative Endometrial Adenocarcinoma Cell Line JEC in vitro
-
Graphical Abstract
-
Abstract
Objective To study the effect of different concentration of estrogen(E2) on the growth of estrogen receptor negative of endometrial adenocarcinoma cell line JEC in vitro. Methods Endometrial adenocarcinoma cell line JEC originated from human endometrial adenocarcinoma was cultured in vitro. Two groups were set up: sample group (17-β estradiol at different concentrations) and control group without estrogen. The proliferative capacity of endometrial adenocarcinoma cell line JEC in the culture medium with 17-β estradiol was assessed by cell counting on a haemocytometer and evaluated by the means of 3-(4,5-dimethylthiazol-z-yl)-2,5-dipheny tertrazolium blue (MTT)and cell cycle was analyzed by flow cytometry (FCM). The expression of cyclin A of JEC was examined by immunocytochemical staining and using automatic image analysis technology. Results (1)The cell numbers in the fourth day after dealing with 1×10-7 and 1×10-6 mol/L concentrations of E2 were more than that in control group. The optical density of JEC cell in the 72th hour after dealing with 1×10-6 mol/L concentration of E2 was higher than that in control group(P<0.01). There was no statistics significant difference in the other experimental groups compared with the control group(P>0.05).(2)FCM showed that 17-β E2(1×10-6mol/L) increased the cells percentage at the S and G2/M phases of cell cycle and decreased the cells percentage in G0/G1 phases of cell cycle.(3)Analysis on expression of intracellular cyclin A protein showed that estradiol could obviously up-regulate cyclin A protein by the immunohistochemical method of SABC. Conclusion It is suggested in the present study that estrogen can stimulate the proliferation of endometrial adenocarcinoma cell line JEC in vitro.There is an accordant dose-response and time-response relationship. In addition, its effect may be associated with the change in the expression of cyclin A.
-
-