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目的 探讨雌激素受体(estrogen receptor, ER)拮抗剂对人子宫内膜样癌(endometrioid carcinoma, EC) JEC细胞(中分化)中ER亚型ERα、ERβ及p57kip2表达的影响.方法 分别用两种ER拮抗剂[他莫昔芬(Tamoxifen, TAM) (10-6 mol/L)、氟维司群(Faslodex,ICI182780) (10-6 mol/L)]及雌二醇(β-Estradiol,E2) ( 10-6 mol/L)干扰 JEC细胞,体外培养 24、48、72 h后,MTT法观察JEC细胞的生长曲线;光镜与电镜观察JEC细胞的形态变化;Western blot法检测JEC细胞中ERα、ERβ及 P57kip2蛋白表达的变化.结果 MTT结果显示,与对照组JEC细胞比较,E2可明显促进JEC细胞增殖,ICI182780则明显抑制 JEC细胞的增殖(P＜0.05);与E2组比较,E2 +ICI182780组JEC细胞增殖能力明显降低(P＜0.05).形态学改变:与对照组比较,E2组细胞密度增大较明显,病理性核分裂象易见ICI182780组细胞密度减小较明显;与E2组比较,E2 +TAM组与E2 + ICI182780组细胞密度均有所减小,核分裂象不易见.Western blot结果显示:与对照组比较,E2组ERβ蛋白表达增高,P57kip2蛋白表达降低(P＜0.05) ;ICI182780组与TAM组ERβ蛋白表达均降低,P57kip2蛋白表达均增高,但仅ICI182780组差异有统计学意义(P＜0.05).与E2组比较,E2 +ICI182780组与E2 +TAM组ERβ蛋白表达均降低,P57kip2蛋白表达均增高,但仅E2+ICI182780组差异有统计学意义(P＜0.05).实验各组及对照组JEC细胞中均无ERα蛋白表达.结论 JEC细胞不表达 ERα蛋白.ICI182780有较强的拮抗雌激素的作用,可能通过下调JEC细胞中ERβ蛋白表达,诱导P57kip2蛋白的表达,发挥其阻滞细胞周期进程的作用,从而抑制肿瘤细胞生长;TAM则对JEC细胞生长有较弱的雌激素样作用.联合检测ERα、ERβ、 P57kip2蛋白在EC中的表达,对EC患者内分泌治疗的个体化选择有重要的参考价值.“,”Purpose To explore the effects of estrogen receptor antagonist on the expression of estrogen receptor subtype (ERα, ERβ), and p57kip2 protein in human endometrioid carcinoma cells named JEC. Methods The JEC cells (moderately differentiated EC cells) cultured in vitro were treated with β-Estradiol (E2) (10～6 mol/L) and two types of estrogen receptor antagonists, tamoxifen (TAM) and fulvestrant (ICI182780) (10-6 mol/L). After 24, 48, 72 h, MTT was used to detect the growth condition of JEC cells, and the light microscopy and electron microscopy were used to observe the growth condition and morphological changes of cells, Western blot was used to detect the expression of ERα, ERβ, PR-A, PR-B and P57kip2 protein in JEC cells. Results MTT results: Compared with the control group, E2 could promote the proliferation of JEC cells significantly (P＜0.05), and ICI182780 could inhibit the proliferation of JEC cells obviously (P＜0.05). Compared with the E2 group, the proliferation ability of JEC cells in E2 + ICI182780 group were lower(P＜0.05). Morphological change: Compared with the control group, the cells density of E2 group increased obviously, and the pathologic mitosis was easy to seen in some cells. The cells density decreased obviously in ICI182780 group. Compared with E2 group, the cells density of E2 + TAM group and E2 + ICI182780 group were decreased, and pathological mitotic figures were difficult to seen. Western blot results: Compared with the control group, the expression of ERβ protein increased, and the expression of p57kip2 protein decreased in E2 group (P＜0.05). The expression of ERβ protein decreased, and the expression of p57kip2 protein increased in ICI182780 group and TAM group, and the difference was statistically significant between ICI182780 group and control group (P＜0.05). Compared with the E2 group, the expression of ERβ protein decreased, and the expression of p57kip2 protein increased in E2 + ICI182780 group and E2 + TAM group, and the difference was statistically significant between E2 + ICI182780 group and E2 group (P＜0.05). ERa protein of JEC cells did not expressed in experimental group or control group. Conclusion ERa protein are not expressed in JEC cells. ICI182780 have a stronger role in antagonizing estrogen, and may induce the expression of p57kip2 protein by down-regulating the expression of ERβ protein in JEC cells, block the cell cycle progression and inhibit the growth of tumor cells. TAM has a weaker estrogen like effect on the growth of JEC cells. It is possible that combined detection of the expression of ERa and p57kip2 protein in EC has an important reference value for individualized selection of endocrine therapy for EC patients.