{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T04:38:03Z","timestamp":1791347883556,"version":"4.3.1"},"reference-count":53,"publisher":"The Endocrine Society","issue":"9","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2013,9,1]]},"abstract":"<jats:p>In hormone-dependent tissues such as breast and ovary, tumorigenesis is associated with an altered expression ratio between the two estrogen receptor (ER) subtypes. In this study, we investigated the effects of ER\u03b2 ectopic expression on 17\u03b2-estradiol (E2)-induced transactivation and cell proliferation in ER\u03b1-positive BG1 ovarian cancer cells. As expected, ER\u03b2 expression strongly decreased the mitogenic effect of E2, significantly reduced E2-dependent transcriptional responses (both on a stably integrated estrogen response element [ERE] reporter gene and on E2-induced mRNAs), and strongly enhanced the formation of ER heterodimers as evidenced by chromatin immunoprecipitation analysis. Inhibition by the ER\u03b1-selective ligand propyl pyrazole triol was less marked than with the pan-agonist (E2) or the ER\u03b2-selective (8\u03b2-vinyl-estradiol) ligands, indicating that ER\u03b2 activation reinforced the inhibitory effects of ER\u03b2. Interestingly, in E2-stimulated BG1 cells, ER\u03b2 was more efficient than ER\u03b1 to regulate the expression of receptor-interacting protein 140 (RIP140), a major ER\u03b1 transcriptional corepressor. In addition, we found that the RIP140 protein interacted better with ER\u03b2 than with ER\u03b1 (both in vitro and in intact cells by fluorescence cross-correlation spectroscopy). Moreover, RIP140 recruitment on the stably integrated reporter ERE was increased upon ER\u03b2 overexpression, and ER\u03b2 activity was more sensitive to repression by RIP140. Finally, small interfering RNA-mediated knockdown of RIP140 expression abolished the repressive effect exerted by activated ER\u03b2 on the regulation of ERE-controlled transcription by estrogens. Altogether, these data demonstrate the inhibitory effects of ER\u03b2 on estrogen signaling in ovarian cancer cells and the key role that RIP140 plays in this phenomenon.<\/jats:p>","DOI":"10.1210\/me.2012-1351","type":"journal-article","created":{"date-parts":[[2013,7,25]],"date-time":"2013-07-25T14:09:23Z","timestamp":1374761363000},"page":"1429-1441","source":"Crossref","is-referenced-by-count":40,"title":["Negative Regulation of Estrogen Signaling by ER\u03b2 and RIP140 in Ovarian Cancer Cells"],"prefix":"10.1210","volume":"27","author":[{"given":"Aur\u00e9lie","family":"Docquier","sequence":"first","affiliation":[{"name":"Institut de Recherche en Canc\u00e9rologie de Montpellier (A.D., A.G., A.B., S.B., V.B., M.B., S.J., P.B., V.C.), Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale (INSERM), U896, Universit\u00e9 Montpellier1, and Institut r\u00e9gional du Cancer Montpellier Montpellier, F-34298, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aur\u00e9lie","family":"Garcia","sequence":"additional","affiliation":[{"name":"Institut de Recherche en Canc\u00e9rologie de Montpellier (A.D., A.G., A.B., S.B., V.B., M.B., S.J., P.B., V.C.), Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale (INSERM), U896, Universit\u00e9 Montpellier1, and Institut r\u00e9gional du Cancer Montpellier Montpellier, F-34298, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julien","family":"Savatier","sequence":"additional","affiliation":[{"name":"Centre de Biochimie Structurale Montpellier (J.S., E.M., C.R.), INSERM U1054, and Centre National de la Recherche Scientifique UMR5048, Universit\u00e9 Montpellier1 and 2, Montpellier, F-34090 France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Abdel","family":"Boulahtouf","sequence":"additional","affiliation":[{"name":"Institut de Recherche en Canc\u00e9rologie de Montpellier 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