Histone deacetylase inhibitors down-regulate G-protein-coupled estrogen receptor and the GPER-antagonist G-15 inhibits proliferation in endometriotic cells

Imesch P, Patrick Imesch, Eleftherios Pierre Samartzis, Eleftherios P Samartzis, Samartzis EP, Konstantin J Dedes, Dedes KJ, Fink D, Daniel Fink, André Fedier
Fertility and sterility · 2013 · vol. 100(3) , pp. 770–776 · doi:10.1016/j.fertnstert.2013.05.008 · PMID:23755949 · W2085730027
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Histone deacetylase inhibitors down-regulate G-protein-coupled estrogen receptor, and the GPER antagonist G-15 inhibits endometriotic cell proliferation.

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Abstract

ObjectiveTo investigate whether histone deacetylase inhibitors reduce the expression of the G-protein-coupled estrogen receptor (GPER) and whether the functional inhibition of GPER by the antagonist G-15 decreases the proliferation of endometriotic cells.DesignIn vitro study.SettingUniversity hospital.Patient(s)Immortalized epithelial endometriotic cells.Intervention(s)Treatment with the histone deacetylase inhibitor romidepsin or suberoylanilide hydroxamic acid (SAHA), or with the GPER antagonist G-15.Main outcome measure(s)Western blot analysis and quantitative real-time polymerase chain reaction (PCR) were used to monitor the expression of GPER in response to drug treatment. Effects of GPER stimulation and inhibition on cell proliferation were investigated by the 93-(4,5-dimethylthiazol-2-yl)2,5-diphenyl tetrazolium bromide (Sigma) (MTT) assay.Result(s)Our results demonstrate that romidepsin and SAHA reduce GPER expression in a concentration-dependent manner. This reduction correlated with the accumulation of acetylated histones. No decreased expression of the estrogen receptor (ER)-α and ERβ was found under comparable experimental conditions. Pretreatment of endometriotic cells with the GPER agonist G-1 stimulated cell proliferation accompanied by rapid Akt phosphorylation. G-15 reversed this stimulation and inhibited cell proliferation, which was accompanied by Akt dephosphorylation.Conclusion(s)G-protein-coupled estrogen receptor is proposed as a potential therapeutic target in endometriosis. The down-regulation of GPER and/or the impairment of its function may reduce the estrogen responsiveness in endometriosis, and therefore might be considered a possible treatment option of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Benzodioxoles Cell Proliferation Endometriosis Histone Deacetylase Inhibitors Quinolines Receptors, Estrogen Receptors, G-Protein-Coupled Benzodioxoles Benzodioxoles Cell Line, Transformed Cell Proliferation Depsipeptides Depsipeptides Depsipeptides Down-Regulation Down-Regulation Down-Regulation Drug Evaluation, Preclinical Endometriosis Endometriosis

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