雌激素效应环指蛋白对子宫内膜癌Ishikawa细胞生长作用及其机制的探讨

Role of Efp on the growth of endometrial carcinoma Ishikawa cells and its meohanism

目的:探讨雌激素效应环指蛋白(Efp)在子宫内膜癌Ishikawa细胞生长中的作用。方法:应用细胞生长试验检测17β-雌二醇(E2)对子宫内膜癌Ishikawa细胞生长的作用,同时应用荧光定量RT-PCR、ELISA和蛋白质印迹法检测E2对子宫内膜癌Ishikawa细胞Efp、VEGF mRNA和蛋白的表达影响,并应用siRNA技术干扰Efp的表达以探讨Efp的作用。结果:E2可以刺激子宫内膜癌Ishikawa细胞的生长,E2(1×10-8mol/L)作用24 h,Efp mRNA和蛋白表达明显升高,约为对照组的2倍,P值分别为0.005和0.038;VEGFmRNA和蛋白表达明显升高,分别为对照组的2.85和2.10倍,P值分别为0.000 8和0.041。当Efp的表达被siRNA抑制后,E2诱导VEGF和对细胞增殖的刺激作用也随之减弱。结论:E2通过Efp作用诱导子宫内膜癌Ishikawa细胞VEGF的产生而调节细胞的生长,Efp可放大雌激素的效应。

OBJECTIVE： To investigate the role of Efp on the growth of endometrial carcinoma Ishikawa cells. METHODS： Growth studies of 17β-estradiol（E2） on endometrial carcinoma Ishikawa cells were performed. The effects of E2 on the induction of VEGF and estrogen-responsive finger protein （Efp） were measured by QRT-PCR and ELISA or western blot. The siRNA method was used to interfere the expression of Efp to investigate the role. RESULTS： E2 induced Ishikawa cell proliferation, the expression of Efp mRNA and protein increased about 2 times with treatment by E2（1 × 10^-8 mol/L ） for 24 h （P= 0. 005, P= 0. 038）, and that of VEGF increased about 2. 85 times （P=0. 000 8） and 2.10 times （P=0. 041） compared with control. When the Efp expression was suppressed by siRNA, the cell growth was decreased with estradiol treatment, and the induction of VEGF by estradiol were decreased. CONCLUSION：These results demonstrate that E2 may regulate the growth of endometrial carcinoma Ishikawa cells by stimulating VEGF production through Efp, and the effects of E2 can be amplified by Efp.