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Role of androgen receptor splice variants in prostate cancer metastasis

Prostate cancer (PCa) is one of the most lethal cancers in western countries. Androgen receptor (AR) signaling pathway plays a key role in PCa progression. Despite the initial effectiveness of androgen deprivation therapy (ADT)for treatment of patients with advanced PCa, most of them will develop re...

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Detalles Bibliográficos
Autores principales: Xu, Jin, Qiu, Yun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Second Military Medical University 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5325179/
https://www.ncbi.nlm.nih.gov/pubmed/28239558
http://dx.doi.org/10.1016/j.ajur.2016.08.003
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author Xu, Jin
Qiu, Yun
author_facet Xu, Jin
Qiu, Yun
author_sort Xu, Jin
collection PubMed
description Prostate cancer (PCa) is one of the most lethal cancers in western countries. Androgen receptor (AR) signaling pathway plays a key role in PCa progression. Despite the initial effectiveness of androgen deprivation therapy (ADT)for treatment of patients with advanced PCa, most of them will develop resistance to ADT and progress to metastatic castration resistant prostate cancer (mCRPC). Constitutively transcriptional activated AR splice variants (AR-Vs) have emerged as critical players in the development and progression of mCRPC. Among AR-Vs identified to date, AR-V7 (a.k.a. AR3) is one of the most abundant and frequently found in both PCa cell lines and in human prostate tissues. Most of functional studies have been focused on AR-V7/AR3 and revealed its role in regulation of survival, growth, differentiation and migration in prostate cells. In this review, we will summarize our current understanding of regulation of expression and activity of AR-Vs in mCRPC.
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spelling pubmed-53251792017-02-24 Role of androgen receptor splice variants in prostate cancer metastasis Xu, Jin Qiu, Yun Asian J Urol Editorial Prostate cancer (PCa) is one of the most lethal cancers in western countries. Androgen receptor (AR) signaling pathway plays a key role in PCa progression. Despite the initial effectiveness of androgen deprivation therapy (ADT)for treatment of patients with advanced PCa, most of them will develop resistance to ADT and progress to metastatic castration resistant prostate cancer (mCRPC). Constitutively transcriptional activated AR splice variants (AR-Vs) have emerged as critical players in the development and progression of mCRPC. Among AR-Vs identified to date, AR-V7 (a.k.a. AR3) is one of the most abundant and frequently found in both PCa cell lines and in human prostate tissues. Most of functional studies have been focused on AR-V7/AR3 and revealed its role in regulation of survival, growth, differentiation and migration in prostate cells. In this review, we will summarize our current understanding of regulation of expression and activity of AR-Vs in mCRPC. Second Military Medical University 2016-10 2016-08-20 /pmc/articles/PMC5325179/ /pubmed/28239558 http://dx.doi.org/10.1016/j.ajur.2016.08.003 Text en © 2016 Editorial Office of Asian Journal of Urology. Production and hosting by Elsevier B.V. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Editorial
Xu, Jin
Qiu, Yun
Role of androgen receptor splice variants in prostate cancer metastasis
title Role of androgen receptor splice variants in prostate cancer metastasis
title_full Role of androgen receptor splice variants in prostate cancer metastasis
title_fullStr Role of androgen receptor splice variants in prostate cancer metastasis
title_full_unstemmed Role of androgen receptor splice variants in prostate cancer metastasis
title_short Role of androgen receptor splice variants in prostate cancer metastasis
title_sort role of androgen receptor splice variants in prostate cancer metastasis
topic Editorial
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5325179/
https://www.ncbi.nlm.nih.gov/pubmed/28239558
http://dx.doi.org/10.1016/j.ajur.2016.08.003
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