Estrogen receptor beta (ER beta) mediates expression of beta-catenin and proliferation in prostate cancer cell line PC-3

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dc.contributor.author Lombardi, Ana Paola G. [UNIFESP]
dc.contributor.author Pisolato, Raisa [UNIFESP]
dc.contributor.author Vicente, Carolina M. [UNIFESP]
dc.contributor.author Lazari, Maria Fatima M. [UNIFESP]
dc.contributor.author Lucas, Thais F. G. [UNIFESP]
dc.contributor.author Porto, Catarina S. [UNIFESP]
dc.date.accessioned 2020-08-14T13:44:13Z
dc.date.available 2020-08-14T13:44:13Z
dc.date.issued 2016
dc.identifier http://dx.doi.org/10.1016/j.mce.2016.04.012
dc.identifier.citation Molecular And Cellular Endocrinology. Clare, v. 430, p. 12-24, 2016.
dc.identifier.issn 0303-7207
dc.identifier.uri https://repositorio.unifesp.br/handle/11600/57539
dc.description.abstract The aim of the present study was to characterize the mechanism underlying estrogen effects on the androgen-independent prostate cancer cell line PC-3. 17 beta-estradiol and the ER beta-selective agonist DPN, but not the ER alpha-selective agonist PPT, increased the incorporation of [methyl-H-3]thymidine and the expression of Cyclin D2, suggesting that ER beta mediates the proliferative effect of estrogen on PC-3 cells. In addition, upregulation of Cyclin D2 and incorporation of [methyl-H-3]thymidine induced by 17 beta-estradiol and DPN were blocked by the ER beta-selective antagonist PHTPP in PC-3 cells. Upregulation of Cyclin D2 and incorporation of [methyl-H-3]thymidine induced by DPN were also blocked by PKF118-310, a compound that disrupts beta-catenin-TCF (T-cell-specific transcription factor) complex, suggesting the involvement of beta-catenin in the estradiol effects in PC-3 cells. A diffuse immunostaining for non-phosphorylated beta-catenin was detected in the cytoplasm of PC-3 cells. Low levels of nonphosphorylated beta-catenin immunostaining were also detected near the plasma membrane and in nuclei. Treatment of PC-3 cells with 17 beta-estradiol or DPN markedly increased non-phosphorylated beta-catenin expression. These effects were blocked by pretreatment with the ER beta-selective antagonist PHTPP, PI3K inhibitor Wortmannin or AKT inhibitor MK-2206, indicating that ER beta-PI3K/AKT mediates non-phosphorylated beta-catenin expression. Cycloheximide blocked the DPN-induced upregulation of nonphosphorylated beta-catenin, suggesting de novo synthesis of this protein. In conclusion, these results suggest that estrogen may play a role in androgen-independent prostate cancer cell proliferation through a novel pathway, involving ER beta-mediated activation of beta-catenin. (C) 2016 Elsevier Ireland Ltd. All rights reserved. en
dc.description.sponsorship Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP)
dc.format.extent 12-24
dc.language.iso eng
dc.publisher Elsevier Ireland Ltd
dc.relation.ispartof Molecular And Cellular Endocrinology
dc.rights Acesso restrito
dc.subject ER beta en
dc.subject beta-catenin en
dc.subject Cyclin D2 en
dc.subject Prostate cancer cells en
dc.title Estrogen receptor beta (ER beta) mediates expression of beta-catenin and proliferation in prostate cancer cell line PC-3 en
dc.type Artigo
dc.description.affiliation Univ Fed Sao Paulo, INFAR, Escola Paulista Med, Sect Expt Endocrinol,Dept Pharmacol, Rua Tres de Maio 100, BR-04044020 Sao Paulo, SP, Brazil
dc.description.affiliationUnifesp Univ Fed Sao Paulo, INFAR, Escola Paulista Med, Sect Expt Endocrinol,Dept Pharmacol, Rua Tres de Maio 100, BR-04044020 Sao Paulo, SP, Brazil
dc.description.sponsorshipID FAPESP: 2008/56564-1
dc.description.sponsorshipID FAPESP: 2014/05292-2
dc.identifier.doi 10.1016/j.mce.2016.04.012
dc.description.source Web of Science
dc.identifier.wos WOS:000378457200002
dc.coverage Clare
dc.citation.volume 430



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