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

dc.citation.volume430
dc.contributor.authorLombardi, Ana Paola Giometti [UNIFESP]
dc.contributor.authorPisolato, Raisa [UNIFESP]
dc.contributor.authorVicente, Carolina Meloni [UNIFESP]
dc.contributor.authorLazari, Maria de Fatima Magalhaes [UNIFESP]
dc.contributor.authorLucas, Thais Fabiana Gameiro [UNIFESP]
dc.contributor.authorPorto, Catarina Segreti [UNIFESP]
dc.coverageClare
dc.date.accessioned2020-08-14T13:44:13Z
dc.date.available2020-08-14T13:44:13Z
dc.date.issued2016
dc.description.abstractThe 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.affiliationUniv 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.affiliationUnifespUniv 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.sourceWeb of Science
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)pt
dc.description.sponsorshipIDFAPESP: 2008/56564-1pt
dc.description.sponsorshipIDFAPESP: 2014/05292-2pt
dc.format.extent12-24
dc.identifierhttps://dx.doi.org/10.1016/j.mce.2016.04.012
dc.identifier.citationMolecular And Cellular Endocrinology. Clare, v. 430, p. 12-24, 2016.
dc.identifier.doi10.1016/j.mce.2016.04.012
dc.identifier.issn0303-7207
dc.identifier.urihttps://repositorio.unifesp.br/handle/11600/57539
dc.identifier.wosWOS:000378457200002
dc.language.isoeng
dc.publisherElsevier Ireland Ltd
dc.relation.ispartofMolecular And Cellular Endocrinology
dc.rightsAcesso restrito
dc.subjectER betaen
dc.subjectbeta-cateninen
dc.subjectCyclin D2en
dc.subjectProstate cancer cellsen
dc.titleEstrogen receptor beta (ER beta) mediates expression of beta-catenin and proliferation in prostate cancer cell line PC-3en
dc.typeArtigo
Arquivos
Coleções