中文摘要：

目的探讨雌激素是否能激活MAPK信号转导通路,以及对子宫内膜癌细胞增殖能力的影响。方法培养子宫内膜癌Ishikawa细胞,按药物干预分为3组：雌二醇（E2）组、U0126（MAPK激酶抑制剂）＋E2组、对照组。采用荧光定量PCR技术检测各组MEK1/2、ERK1/2 m RNA表达的变化;Western blot法检测各组p-MEK1/2、p-ERK1/2蛋白的活化程度;流式细胞仪检测各组的细胞周期比例;细胞集落形成实验检测各组细胞的增殖能力;体外穿膜实验比较各组细胞的迁移能力。结果 E2组MEK1/2、ERK1/2 m RNA表达增加（P=0.025,P=0.002）,U0126＋E2组中,U0126能阻断E2诱导MEK1/2、ERK1/2m RNA的表达上调（P=0.000,P=0.000）。E2组p-MEK1/2、p-ERK1/2蛋白活化水平升高（P=0.049,P=0.028）;U0126＋E2组中,U0126能阻断E2诱导的p-MEK1/2、p-ERK1/2蛋白活化（P=0.018,P=0.003）。E2组G1期细胞比例显著低于对照组及U0126＋E2组（P=0.017）,集落形成率显著高于对照组及U0126＋E2组（P=0.009）,穿过微孔的细胞数显著多于对照组及U0126＋E2组（P=0.000）。结论雌二醇通过激活MAPK通路,促进子宫内膜癌的发展,MEK抑制剂能阻断并抑制这一作用。

英文摘要：

Objective To explore whether estradiol could activate the mitogen-activated protein kinase（MAPK） pathway and its effect on the proliferation of endometrial cancer Ishikawa cells. Methods Endometrial cancer Ishikawa cells were divided into three groups： estradiol（E2） group, U0126（MAPK inhibitor）＋E2 group and control group. The expression of MEK1/2 and ERK1/2 m RNA were determined by q RT-PCR. The activation states of p-ERK1/2 and p-MEK1/2 protein were analyzed by Western blot. Flow cytometry was used to examine the cell cycle. Colony formation ability was detected by colony formation assay. Transwell assay was used to detect the cell migration. Results E2 significantly increased the expression of MEK1/2 and ERK1/2 m RNA（P=0.025, P=0.002）. In the U0126＋E2 group, U0126 signifi cantly inhibited the up-regulation of MEK1/2, ERK1/2 m RNA expression induced by E2（P=0.000, P=0.000）. E2 increased the activation level of p-MEK1/2, p-ERK1/2 protein（P=0.049, P=0.028）. In the U0126＋E2 group, U0126 signifi cantly inhibited the up-regulation of p-MEK1/2 and p-ERK1/2 protein activation levels induced by E2（P=0.018, P=0.003）. Compared with the U0126＋E2 group and control group, the cells at G1 stage were less. the colony forming rate was lower and the cells migration ability was higher in E2 group（P=0.017, P=0.009, P=0.000）. Conclusion Estradiol could activate MAPK pathway and promote the development of endometrial cancer cells. However, MEK inhibitor could block and inhibit this effect.