重庆医学2017，Vol.46Issue(9)：1168-1171,4.DOI:10.3969/j.issn.1671-8348.2017.09.005
新型雌激素受体GPR30激活HER2-ERK1/2促进乳腺癌MCF-7细胞迁移和侵袭
GPR30 promotes MCF-7 breast cancer cell migration and invasion by activating HER2-ERK1/2 signaling pathway
摘要
Abstract
Objective To study the molecular mechanism and biological significance of GPR30 activating HER2 in MCF-7 breast cancer cells with low expresses HER2.Methods Western blot was adopted to examine the phosphorylation of HER2 and the downstream signaling molecular ERK1/2 after 17-β-estradiol(E2),4-OHT(the active metabolite of tamoxifen) or G-1 (the GPR30 agonist) treatment in MCF-7 cells.After different inhibitors such as G-15 (the GPR30 antagonist),AG1478(EGFR tyrosine inhibitor),AG825 (HER2 tyrosine inhibitor),PP2 (Src family kinase inhibitor)or GM6001 (MMP inhibitor) pretreated for 2 h,the phosphorylation of HER2 and ERK1/2 were further analyzed.Finally,the altered migration and invasive capability of MCF-7 cells were detected by Transwell method.Results HER2 and ERK1/2 were activated in MCF-7 cells after E2,4-OHT or G-1 treatment and these changes could be inhibited by G-15,AG1478,AG825,PP2 or GM6001 pretreatment.The enhancement of G-1-induced migration and invasion ability in MCF-7 cells could also be inhibited by those inhibitors too.Conclusion GPR30 promotes the migration and invasion of MCF-7 cells through activating HER2-ERK1/2 signal transduction pathway.关键词
乳腺肿瘤/G蛋白耦联受体30/表皮生长因子受体2/细胞运动/侵袭Key words
breast neoplasms/G protein-coupled receptor 30/human epidermal growth factor receptor-2/cell movement/invasion分类
医药卫生引用本文复制引用
阮姝琴,代晓燕..新型雌激素受体GPR30激活HER2-ERK1/2促进乳腺癌MCF-7细胞迁移和侵袭[J].重庆医学,2017,46(9):1168-1171,4.基金项目
2013年重庆市卫生局医学科研资助项目(2013-2-111) （2013-2-111）
2013年重庆市渝中区科技计划项目(20130144). （20130144）
