Sun Peng-Ming, Wei Li-Hui, Gao Min, Wang Jian-Liu, Zhao Li-Jun, Wang Da-Peng, Zhang Jun-Xiao
Department of Obstetrics and Gynecology, Peking University People's Hospital, Beijing 100044, China.
Zhonghua Fu Chan Ke Za Zhi. 2007 Jun;42(6):408-11.
To investigate the role of human estrogen receptor-related receptor (ERR) alpha, a submember of orphan receptors, in the tumorigenesis of endometrial cancer.
Plasmid of pSG-ERRalpha was transfected into endometrial cancer cell lines HEC-1A, HEC-1B, and Ishikawa. Real-time quantitative RT-PCR and western blot were used to analyze the mRNA and protein expression of ERRalpha in endometrial cancer cell. Flow cytometry was used to analyze the cellular growth.
Expressions of the ERRalpha were significantly increased in the endometrial cancer cells transfected with pSG-ERRalpha plasmid; expression of the ERRalpha mRNA in HEC-1A cell was 9644.4 copies/ng, HEC-1B: 9835.3 copies/ng, and Ishikawa: 8008.6 copies/ng (P < 0.01); expression of the ERRalpha protein in HEC-1A cell was 1.128, HEC-1B: 1.104, and Ishikawa: 1.008 (P < 0.05). Flow cytometry showed over-expression of ERRalpha was accompanied by increased HEC-1A and HEC-1B cells in S and G(2)/M phase (P < 0.01), while this could not be observed in the estrogen receptor (ER) positive endometrial cancer cell line Ishikawa. Furthermore, cellular growth analysis showed that over-expression of ERRalpha induced cell growth increase of the ER negative endometrial cancer cells HEC-1A and HEC-1B (P < 0.05).
Over-expression of ERRalpha could stimulate ER negative endometrial cancer cell proliferation independent of estrogen-ER pathway.
研究孤儿受体亚成员人类雌激素受体相关受体(ERR)α在子宫内膜癌发生中的作用。
将pSG-ERRα质粒转染至子宫内膜癌细胞系HEC-1A、HEC-1B和Ishikawa。采用实时定量逆转录聚合酶链反应(RT-PCR)和蛋白质免疫印迹法分析ERRα在子宫内膜癌细胞中的mRNA和蛋白表达。采用流式细胞术分析细胞生长情况。
转染pSG-ERRα质粒的子宫内膜癌细胞中ERRα表达显著增加;HEC-1A细胞中ERRα mRNA表达为9644.4拷贝/ng,HEC-1B为9835.3拷贝/ng,Ishikawa为8008.6拷贝/ng(P<0.01);HEC-1A细胞中ERRα蛋白表达为1.128,HEC-1B为1.104,Ishikawa为1.008(P<0.05)。流式细胞术显示,ERRα过表达伴随着HEC-1A和HEC-1B细胞S期和G(2)/M期增加(P<0.01),而在雌激素受体(ER)阳性的子宫内膜癌细胞系Ishikawa中未观察到此现象。此外,细胞生长分析显示,ERRα过表达诱导ER阴性的子宫内膜癌细胞HEC-1A和HEC-1B细胞生长增加(P<0.05)。
ERRα过表达可独立于雌激素-ER途径刺激ER阴性的子宫内膜癌细胞增殖。