Expression and regulation of the estrogen receptors in PC-3 human prostate cancer cells

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dc.citation.volume107
dc.contributor.authorPisolato, Raisa [UNIFESP]
dc.contributor.authorLombardi, Ana Paola Giometti [UNIFESP]
dc.contributor.authorVicente, Carolina Meloni [UNIFESP]
dc.contributor.authorLucas, Thais Fabiana Gameiro [UNIFESP]
dc.contributor.authorLazari, Maria de Fatima Magalhaes [UNIFESP]
dc.contributor.authorPorto, Catarina Segreti [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.coverageNew York
dc.date.accessioned2020-08-21T17:00:08Z
dc.date.available2020-08-21T17:00:08Z
dc.date.issued2016
dc.description.abstractThe aim of this study was to identify the expression, cellular localization and regulation of classic estrogen receptors ER alpha, and ER beta, ER-alpha 36 isoform and GPER in the androgen-independent prostate cancer cell line PC-3. In addition, we evaluated the relative contribution of these receptors to the activation of the ERK1/2 (extracellular signal-regulated protein kinases) signaling pathway. These four estrogen receptors were detected by Western blot assays and were shown by immunofluorescence assays to localize preferentially in extranuclear regions of PC-3 cells. In addition, treatment with 17 beta-estradiol (E2) (1 mu M) for 24 h led to down-regulation of the classic estrogen receptors, whereas E2 at physiological concentration (0.1 nM) for 24 h tended to increase the levels of ER alpha and ER beta. Furthermore, the ER alpha-selective agonist PPT selectively increased the expression of ER beta and the ER beta-selective agonist DPN increased ER alpha levels. None of these treatments affected expression of the ER-alpha 36 isoform. The unusual cytoplasmic localization of the classic estrogen receptors in these cells differs from the nuclear localization in the majority of estrogen target cells and suggests that rapid signaling pathways may be preferentially activated. In fact, treatment with selective agonists of ER alpha, ER beta and GPER induced ERK1/2 phosphorylation that was blocked by the respective antagonists. On the other hand, activation of ERK1/2 induced by E2 may involve additional mechanisms because it was not blocked by the three antagonists. Taken together, the results indicate that there is a crosstalk between ER alpha and ER beta to regulate the expression of each other, and suggest the involvement of other receptors, such as ER-alpha 36, inthe rapid ERK1/2 activation by E2. The identification of new isoforms of-ERs, regulation of the receptors and signaling pathways is important to develop new therapeutic strategies for the castration-resistant prostate cancer. (C) 2016 Elsevier Inc. All rights reserved.en
dc.description.affiliationUniv Fed Sao Paulo, Dept Pharmacol, Sect Expt Endocrinol, Escola Paulista Med, Sao Paulo, SP, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo, Dept Pharmacol, Sect Expt Endocrinol, Escola Paulista Med, Sao Paulo, SP, Brazil
dc.description.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt
dc.description.sponsorshipCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)pt
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)pt
dc.description.sponsorshipIDFAPESP: 2008/56564-1pt
dc.format.extent74-86
dc.identifierhttps://dx.doi.org/10.1016/j.steroids.2015.12.021
dc.identifier.citationSteroids. New York, v. 107, p. 74-86, 2016.
dc.identifier.doi10.1016/j.steroids.2015.12.021
dc.identifier.issn0039-128X
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/57880
dc.identifier.wosWOS:000372564000009
dc.language.isoeng
dc.publisherElsevier Science Inc
dc.relation.ispartofSteroids
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectEstrogen receptors alpha and betaen
dc.subjectER-alpha 36en
dc.subjectGPERen
dc.subjectERK1/2en
dc.subjectPC-3 cellsen
dc.titleExpression and regulation of the estrogen receptors in PC-3 human prostate cancer cellsen
dc.typeinfo:eu-repo/semantics/article
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