Advanced search
Start date
Betweenand
(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Activation of estrogen receptor beta (ER beta) regulates the expression of N-cadherin, E-cadherin and beta-catenin in androgen-independent prostate cancer cells

Full text
Author(s):
Silva, Rafael de Souza [1] ; Lombardi, Ana Paola G. [1] ; de Souza, Deborah Simao [1] ; Vicente, Carolina M. [1] ; Porto, Catarina S. [1]
Total Authors: 5
Affiliation:
[1] Univ Fed Sao Paulo, Escola Paulista Med, Dept Pharmacol, Sect Expt Endocrinol, Rua Pedro de Toledo 669, BR-04039032 Sao Paulo, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY; v. 96, p. 40-50, MAR 2018.
Web of Science Citations: 3
Abstract

The aim of the present study was to investigate the impact of the activation of estrogen receptors on expression and localization of N-cadherin, E-cadherin and non-phosphorylated beta-catenin in androgen-independent prostate cancer cells (PC-3 and DU-145) and in human post pubertal prostate epithelial cells (PNT1A). Expression of N-cadherin was detected in PNT1A and PC-3 cells, but not in DU-145 cells. E-cadherin was detected only in DU-145 cells and beta-catenin was detected in all cells studied. N-cadherin and beta-catenin were located preferentially in the cellular membrane of PNT1A cells and in the cytoplasm of PC-3 cells. E-cadherin and beta-catenin were located preferentially in the cellular membrane of DU-145 cells. 17 beta-estradiol (E2) or the ER alpha-selective agonist PPT did not affect the content and localization of N-cadherin in PC-3 and PNT1A cells or E-cadherin in DU-145 cells. In PC-3 cells, ER beta-selective agonist DPN decreased the expression of N-cadherin. DPN-induced downregulation of N-cadherin was blocked by pretreatment with the ER beta-selective antagonist (PHTPP), indicating that ER beta 1 is the upstream receptor regulating the expression of N-cadherin. In DU-145 cells, the activation of ER beta 1 by DPN increased the expression of E-cadherin. Taken together, these results suggest that activation of is required to maintain an epithelial phenotype in PC-3 and DU-145 cells. The activation of ER beta 1 also increased the expression of beta-catenin in cytoplasm of PC-3 and in the cellular membrane of DU-145 cells. In conclusion, our results indicate differential expression and localization of N-cadherin, E-cadherin and beta-catenin in androgen independent prostate cancer cells. The reduction of N-cadherin content by activation of ER beta, exclusively observed in androgen-independent prostate cancer cells (PC-3), may be related to the activation of signaling pathways, such as the release of beta-catenin into the cytoplasm, translocation of beta-catenin to the nucleus and activation of gene transcription. (AU)

FAPESP's process: 14/05292-2 - Estrogen receptors and intracellular signaling pathways involved in the regulation of cell proliferation of testicular cancer and castration-resistant prostate cancer
Grantee:Catarina Segreti Porto
Support type: Regular Research Grants