当前位置： SCI文献检索 > CELL BIOLOGY INTERNATIONAL期刊下所有文献 > A novel estrogen receptor GPER mediates proliferation induced by 17β-estradiol and selective GPER agonist G-1 in estrogen receptor α (ERα)-negative ovarian cancer cells.

A novel estrogen receptor GPER mediates proliferation induced by 17β-estradiol and selective GPER agonist G-1 in estrogen receptor α (ERα)-negative ovarian cancer cells.

Abstract：

:G protein-coupled estrogen receptor (GPER) is recently identified as a membrane-associated estrogen receptor that mediates non-genomic effects of estrogen. Our previous immunohistochemistry study found an association between GPER and the proliferation of epithelial ovarian cancer. However, the contributions and mechanisms of GPER in the proliferation of ovarian cancers are not clear. We have examined the role of GPER in estrogen receptor α (ERα)-negative/GPER positive OVCAR5 ovarian cancer cell line. MTT assay was used to detect cell proliferation. BrdU incorporation assay was used to measure the cells in S-phase. Protein expression of marker genes of proliferation, cell cycle and apoptosis were examined by Western blot. The results showed that 17β-estradiol and selective GPER agonist G-1 stimulated the proliferation of OVCAR5 cells and increased the cells in S-phase. Both ligands upregulated the protein levels of c-fos and cyclin D1. Small interfering RNA targeting GPER or G protein inhibitor pertussin toxin (PTX) inhibited basal cell proliferation and attenuated 17β-estradiol- or G-1-induced cell proliferation. GPER mediated cell growth was also associated with the apoptosis of OVCAR5 cells. These findings suggest that GPER has an important function in the proliferation of ovarian cancer cells lacking ERα. GPER might be a promising therapeutic target in ovarian cancer.

journal_name

Cell Biol Int

journal_title

Cell biology international

authors

Liu H,Yan Y,Wen H,Jiang X,Cao X,Zhang G,Liu G

doi

10.1002/cbin.10243

subject

Has Abstract

pub_date

2014-05-01 00:00:00

pages

631-8

issue

5

eissn

1065-6995

issn

1095-8355

journal_volume

38

pub_type

杂志文章

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