子宫内膜腺癌组织中人类RUNT相关转录因子3与果蝇zeste基因增强子同源物2的表达

Expression of RUNX3 and EZH2 in endometrial adenocarcinoma tissue

目的:检测子宫内膜腺癌组织中人类RUNT相关转录因子3(RUNX3)和果蝇zeste基因增强子同源物2(EZH2)的表达。方法:采用免疫组化SP法检测60例子宫内膜腺癌、40例子宫内膜增殖症和20例正常增生期子宫内膜组织中RUNX3与EZH2蛋白的表达。结果:子宫内膜腺癌、子宫内膜增殖症与正常增生期子宫内膜组织RUNX3蛋白的阳性表达率分别为43.3%(26/60)、67.5%(27/40)与95.0%(19/20),3组间相比,差异有统计学意义(χ2=18.090,P<0.001);上述3种组织中EZH2蛋白的阳性表达率分别为75.0%(45/60)、42.5%(17/40)与15.0%(3/20),3组间相比,差异有统计学意义(χ2=25.041,P<0.001)。RUNX3蛋白的表达与子宫内膜腺癌的组织分化程度、TNM分期及浸润深度有关(χ2=-3.561,-2.367,5.370,P均<0.05),EZH2蛋白的表达与子宫内膜腺癌的组织分化程度及浸润深度有关(χ2=-3.084,5.568,P均<0.05)。子宫内膜腺癌组织中RUNX3和EZH2蛋白的表达相关(rP=0.330,P=0.007)。结论:RUNX3蛋白表达缺失和EZH2蛋白过度表达在子宫内膜腺癌的发生与发展中起重要作用,高表达的EZH2可能在一定程度上参与调控RUNX3基因的表达下调。

Aim：To investigate the roles and correlation of RUNX3 and EZH2 in pathogenesis and development of endometrial adenocarcinoma.Methods：The expressions of RUNX3 and EZH2 in endometrial adenocarcinomas（60 cases）,endometrial hyperplasia（40 cases） and normal endometrium at proliferative phase（20 cases） tissue were detected by immunohistochemical SP method.Results：In endometrial adenocarcinoma,endometrial hyperplasia and normal endometrium,the positive rates of RUNX3 expression were 43.3%（26/60）,67.5%（27/40）,and 95.0%（19/20）,and there were significant differences among the 3 groups（χ2=18.090,P0.001）.The positive rates of EZH2 expression were 75.0%（45/60）,42.5%（17/40）,and 15.0%（3/20）,and there were significant differences among the 3 groups（χ2=25.041,P0.001）.In endometrial adenocarcinoma tissue,the expression of RUNX3 was related with histological grade,progression of clinical stage and depth of myometrial invasion（χ2=-3.561,-2.367,5.370,P0.05）;the expressions of EZH2 was related with histological grade and depth of myometrial invasion（χ2=-3.084,5.568,P0.05）;the expressions of RUNX3 and EZH2 were negatively correlated（rP=0.330,P=0.007）.Conclusion：RUNX3 inactivation and EZH2 overexpression may play important roles in the carcinogenesis and development of endometrial adenocarcinoma,and the overexpression of EZH2 may be involved in the inactivation of RUNX3 expression.