Estrogenic transmembrane receptor of GPR30 mediates invasion and carcinogenesis by endometrial cancer cell line RL95-2

被引:38
作者
He, Yin-Yan [2 ]
Du, Gui-Qiang [1 ]
Cai, Bin [2 ]
Yan, Qin [1 ]
Zhou, Long [1 ]
Chen, Xiao-Yue [1 ]
Lu, Wen [1 ]
Yang, Yi-Xia [2 ]
Wan, Xiao-Ping [1 ]
机构
[1] Shanghai Jiao Tong Univ, Dept Obstet & Gynecol, Int Peace Matern & Child Hlth Hosp China, Welf Inst, Shanghai 200030, Peoples R China
[2] Shanghai Jiao Tong Univ, Dept Obstet & Gynecol, Shanghai Peoples Hosp 1, Shanghai 200030, Peoples R China
基金
中国博士后科学基金; 中国国家自然科学基金;
关键词
Endometrial cancer; GPR30; Carcinogenesis; Estrogen; Estrogen receptor; PROTEIN-COUPLED RECEPTOR; GROWTH-FACTOR RECEPTOR; BREAST-CANCER; EXPRESSION; G-PROTEIN-COUPLED-RECEPTOR-30; 17-BETA-ESTRADIOL; PROLIFERATION; EXTRANUCLEAR;
D O I
10.1007/s00432-011-1133-7
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The mechanisms underlying the effects of estrogen on endometrial cancer remain undefined. Although the classical mechanism of the action of estrogen involves binding to the estrogen receptors alpha and beta, and transduction of the signal into the cell, G protein-coupled receptor (GPR) 30 has been shown to mediate nongenomic estrogen signaling. The goal of this study was to determine the role of GPR30 signal in the basic process such as invasion and carcinogenesis of endometrial cancer. We downregulated the expression of GPR30 in endometrial cancer cell line RL95-2 by transfection with shGPR30-pGFP-V-RS, a GPR30 antisense expression vector. The cells were then subjected to an MTT assay and a Transwell(A (R)) migration assay. And an animal model was also used to investigate the influence of downregulation of GPR30 on oncogenesis. Downregulation of GPR30 led to reduced growth and invasion by cells treated with 17 beta-estradiol. And the capacity of transfected RL95-2 cells to promote tumorigenesis was weakened in vivo. Our data suggest that, for the endometrial cancer cell line RL95-2, GPR30 plays important roles in mediating the proliferative and invasive effects of estrogen and in tumorigenesis.
引用
收藏
页码:775 / 783
页数:9
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