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Estrogen receptor {beta}1 exerts antitumoral effects on SK-OV-3 ovarian cancer cells
Oliver Treeck1, Georg Pfeiler, Diana Mitter
1Department of Obstetrics and Gynecology, Klinik für Frauenheilkunde und Geburtshilfe, University of Regensburg, Landshuter Strasse 65, 93053 Regensburg, Germany. otreeck@caritasstjosef.de
Abstract:
Estrogen receptor (ER) beta1 and its splice variants are expressed both in ovary and ovarian cancer. We studied the role of ERbeta1 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 ERbeta1 or its splice variants ERbeta-delta125 and ERbeta-delta1256, and tested their response to estrogen and tamoxifen in comparison with the untransfected cells. Heterologous expression of ERbeta1, but not of the exon-deleted ERbeta 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 ERbeta1 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 ERbeta1, 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 ERalpha.
Insights
Estrogen receptor beta1 (ERbeta1) exhibits anti-tumor effects in ovarian cancer cells by slowing growth and increasing apoptosis. These benefits occur independently of estradiol, highlighting ERbeta1
Area of Science:
- Oncology
- Molecular Biology
- Endocrinology
Background:
- Estrogen receptor (ER) beta1 and its splice variants are present in ovarian tissues and ovarian cancer.
- The specific roles of ERbeta1 and its variants in ovarian cancer progression are not fully understood.
Purpose of the Study:
- To investigate the functional roles of ERbeta1 and its splice variants (ERbeta-delta125, ERbeta-delta1256) in regulating gene expression, proliferation, apoptosis, and migration in an ovarian cancer cell line.
- To compare the effects of ERbeta1 and its variants on SK-OV-3 cells in response to estrogen and tamoxifen.
Main Methods:
- Transfection of SK-OV-3 ovarian cancer cells with vectors encoding ERbeta1, ERbeta-delta125, or ERbeta-delta1256.
- Assessment of cellular proliferation, apoptosis, and migration.
- Analysis of gene expression levels for key regulatory molecules (e.g., p21(WAF1), cyclin A2, fibulin 1c).
Main Results:
- ERbeta1 expression significantly reduced SK-OV-3 cell growth, increased apoptosis, and decreased cell motility.
- These effects were associated with increased p21(WAF1) transcript levels and decreased cyclin A2 mRNA levels.
- ERbeta1 mediated these anti-tumoral effects independently of estradiol or ERalpha, whereas exon-deleted variants did not.
Conclusions:
- ERbeta1 possesses significant anti-tumoral properties in ovarian cancer cells, including inhibition of proliferation and migration, and promotion of apoptosis.
- The anti-cancer effects of ERbeta1 are mediated through specific molecular pathways and are independent of canonical estrogen signaling.
- Exon-deleted ERbeta variants lack the anti-tumoral activity observed for ERbeta1, suggesting isoform-specific functions.
