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

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dc.contributor.author Pisolato, R. [UNIFESP]
dc.contributor.author Lombardi, A. P. G. [UNIFESP]
dc.contributor.author Vicente, C. M. [UNIFESP]
dc.contributor.author Lucas, T. F. G. [UNIFESP]
dc.contributor.author Lazari, M. F. M. [UNIFESP]
dc.contributor.author Porto, C. S. [UNIFESP]
dc.date.accessioned 2020-08-21T17:00:08Z
dc.date.available 2020-08-21T17:00:08Z
dc.date.issued 2016
dc.identifier http://dx.doi.org/10.1016/j.steroids.2015.12.021
dc.identifier.citation Steroids. New York, v. 107, p. 74-86, 2016.
dc.identifier.issn 0039-128X
dc.identifier.uri https://repositorio.unifesp.br/handle/11600/57880
dc.description.abstract The 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.sponsorship FAPESP - Brazil
dc.description.sponsorship CAPES/PNPD - Brazil
dc.description.sponsorship CNPq - Brazil
dc.description.sponsorship FAPESP
dc.format.extent 74-86
dc.language.iso eng
dc.publisher Elsevier Science Inc
dc.relation.ispartof Steroids
dc.rights Acesso restrito
dc.subject Estrogen receptors alpha and beta en
dc.subject ER-alpha 36 en
dc.subject GPER en
dc.subject ERK1/2 en
dc.subject PC-3 cells en
dc.title Expression and regulation of the estrogen receptors in PC-3 human prostate cancer cells en
dc.type Artigo
dc.description.affiliation Univ Fed Sao Paulo, Dept Pharmacol, Sect Expt Endocrinol, Escola Paulista Med, Sao Paulo, SP, Brazil
dc.description.affiliationUnifesp Univ Fed Sao Paulo, Dept Pharmacol, Sect Expt Endocrinol, Escola Paulista Med, Sao Paulo, SP, Brazil
dc.description.sponsorshipID FAPESP: 2008/56564-1
dc.identifier.doi 10.1016/j.steroids.2015.12.021
dc.description.source Web of Science
dc.identifier.wos WOS:000372564000009
dc.coverage New York
dc.citation.volume 107



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