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shanghai “post-qi-ming-xing plan” shgpr30-pgfp-v-rs wen lu & xiao-ping wan month download article/chapter protein-coupled receptor homolog protein-coupled estrogen receptor protein-coupled receptor gpr30 membrane¨cspanning estrogen receptor xiao-ping wan estrogenic transmembrane receptor protein-coupled receptor protein–coupled receptor 30 protein-coupled receptor 30 full article pdf estrogen receptors α functional estrogen receptors clinical oncology aims related subjects gpr30 estrogen receptor endometrial cancer cells transfected rl95-2 cells privacy choices/manage cookies estrogen receptor expression mapk signaling axis xiao-yue chen china yin-yan ovarian cancer cells thyroid cancer cells primary breast cancer estrogen involves binding estrogen dendrimer conjugates gui-qiang du mediates gene expression ligand-induced homodimer estrogen-induced activation gpr30 mediates invasion estrogen receptors european economic area short hairpin rna hush 29-mer noneffective frackelton ar jr camp-mediated attenuation dipeptidyl peptidase iv international peace maternity du contributed equally conditions privacy policy transwell® migration assay child health hospital article journal endometrial cancer

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         description: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 α and β, 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® 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 17β-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.
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