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Department of Obstetrics and Gynecology, Klinik für Frauenheilkunde und Geburtshilfe, University of Regensburg, Landshuter Strasse 65, 93053 Regensburg, Germany

(Requests for offprints should be addressed to O Treeck; Email: otreeck{at}caritasstjosef.de)

^* (O Treeck and G Pfeiler contributed equally to this study)

Estrogen receptor (ER) ß1 and its splice variants are expressed both in ovary and ovarian cancer. We studied the role of ERß1 and two of its splice variants in regulation of gene expression, cellular proliferation, apoptosis, and migration of an ovarian cancer cell line. In this study, we transfected SK-OV-3 ovarian cancer cells with vectors coding for ERß1 or its splice variants ERß-125 and ERß-1256, and tested their response to estrogen and tamoxifen in comparison with the untransfected cells. Heterologous expression of ERß1, but not of the exon-deleted ERß variants resulted in notably slower cell growth of SK-OV-3 ovarian cancer cells, an effect accompanied by more than tenfold increase of cyclin-dependent kinase inhibitor p21(WAF1) transcript levels and a significant reduction of cyclin A2 mRNA levels. SK-OV-3 cells stably overexpressing ERß1 ligand independently also exhibited an increased apoptosis rate and a significantly decreased motility, an effect accompanied by upregulation of fibulin 1c. Our data demonstrate that ERß1, but not the exon-deleted isoforms tested exerts multiple antitumoral effects on SK-OV-3 ovarian cancer cells even in the absence of estradiol or functional ER.

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