ERβ- and Prostaglandin E2-Regulated Pathways Integrate Cell Proliferation via Ras-like and Estrogen-Regulated Growth Inhibitor in Endometriosis

D Monsivais, Diana Monsivais, Monsivais D, M T Dyson, Matthew T. Dyson, Yin P, Ping Yin, P Yin, Coon JS, John S. Coon, J S Coon, A Navarro, Antònia Navarro, Navarro A, Feng G, G Feng, Gang Feng, S S Malpani, Malpani SS, Saurabh Malpani, Masanori Ono, M Ono, Ercan CM, C M Ercan, Cihangir Mutlu Ercan, Jian Wei, J J Wei, Wei JJ, Mary Ellen Pavone, Pavone ME, M E Pavone, Su E, Emily Su, E Su, Serdar E. Bulun, S E Bulun, Bulun Se
Molecular Endocrinology · 2014 · vol. 28(8) , pp. 1304–1315 · doi:10.1210/me.2013-1421 · PMID:24992181 · PMC4116594 · W2010229505
article OA: bronze CC0 ⤵ 58 in-corpus citations
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Estradiol/ERβ and prostaglandin E2 pathways converge on RERG to promote endometriotic cell proliferation, identifying RERG as a potential therapeutic target.

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Abstract

In endometriosis, stromal and epithelial cells from the endometrium form extrauterine lesions and persist in response to estrogen (E2) and prostaglandin E2 (PGE2). Stromal cells produce excessive quantities of estrogen and PGE2 in a feed-forward manner. However, it is unknown how estrogen stimulates cell proliferation and survival for the establishment and persistence of disease. Previous studies suggest that estrogen receptor-β (ERβ) is strikingly overexpressed in endometriotic stromal cells. Thus, we integrated genome-wide ERβ binding data from previously published studies in breast cells and gene expression profiles in human endometriosis and endometrial tissues (total sample number = 81) and identified Ras-like, estrogen-regulated, growth inhibitor (RERG) as an ERβ target. Estradiol potently induced RERG mRNA and protein levels in primary endometriotic stromal cells. Chromatin immunoprecipitation demonstrated E2-induced enrichment of ERβ at the RERG promoter region. PGE2 via protein kinase A phosphorylated RERG and enhanced the nuclear translocation of RERG. RERG induced the proliferation of primary endometriotic cells. Overall, we demonstrated that E2/ERβ and PGE2 integrate at RERG, leading to increased endometriotic cell proliferation and represents a novel candidate for therapeutic intervention.

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Condition tags

endometriosis

MeSH descriptors

Cell Proliferation Dinoprostone Endometriosis Estrogen Receptor beta GTP Phosphohydrolases Adult Cell Nucleus Cell Nucleus Dinoprostone Endometriosis Endometriosis Estradiol Estradiol Estrogen Receptor beta Female Gene Expression Regulation GTP Phosphohydrolases HEK293 Cells Humans Protein Transport

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