Molecular mechanisms of docetaxel resistance in prostate cancer

Docetaxel (DTX) chemotherapy offers excellent initial response and confers significant survival benefit in patients with castration-resistant prostate cancer (CRPC). However, the clinical utility of DTX is compromised when primary and acquired resistance are encountered. Therefore, a more thorough u...

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Detalles Bibliográficos
Autores principales: Sekino, Yohei, Teishima, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: OAE Publishing Inc. 2020
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992564/
https://www.ncbi.nlm.nih.gov/pubmed/35582222
http://dx.doi.org/10.20517/cdr.2020.37
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author Sekino, Yohei
Teishima, Jun
author_facet Sekino, Yohei
Teishima, Jun
author_sort Sekino, Yohei
collection PubMed
description Docetaxel (DTX) chemotherapy offers excellent initial response and confers significant survival benefit in patients with castration-resistant prostate cancer (CRPC). However, the clinical utility of DTX is compromised when primary and acquired resistance are encountered. Therefore, a more thorough understanding of DTX resistance mechanisms may potentially improve survival in patients with CRPC. This review focuses on DTX and discusses its mechanisms of resistance. We outline the involvement of tubulin alterations, androgen receptor (AR) signaling/AR variants, ERG rearrangements, drug efflux/influx, cancer stem cells, centrosome clustering, and phosphoinositide 3-kinase/AKT signaling in mediating DTX resistance. Furthermore, potential biomarkers for DTX treatment and therapeutic strategies to circumvent DTX resistance are reviewed.
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spelling pubmed-89925642022-05-16 Molecular mechanisms of docetaxel resistance in prostate cancer Sekino, Yohei Teishima, Jun Cancer Drug Resist Review Docetaxel (DTX) chemotherapy offers excellent initial response and confers significant survival benefit in patients with castration-resistant prostate cancer (CRPC). However, the clinical utility of DTX is compromised when primary and acquired resistance are encountered. Therefore, a more thorough understanding of DTX resistance mechanisms may potentially improve survival in patients with CRPC. This review focuses on DTX and discusses its mechanisms of resistance. We outline the involvement of tubulin alterations, androgen receptor (AR) signaling/AR variants, ERG rearrangements, drug efflux/influx, cancer stem cells, centrosome clustering, and phosphoinositide 3-kinase/AKT signaling in mediating DTX resistance. Furthermore, potential biomarkers for DTX treatment and therapeutic strategies to circumvent DTX resistance are reviewed. OAE Publishing Inc. 2020-08-21 /pmc/articles/PMC8992564/ /pubmed/35582222 http://dx.doi.org/10.20517/cdr.2020.37 Text en © The Author(s) 2020. https://creativecommons.org/licenses/by/4.0/© The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.
spellingShingle Review
Sekino, Yohei
Teishima, Jun
Molecular mechanisms of docetaxel resistance in prostate cancer
title Molecular mechanisms of docetaxel resistance in prostate cancer
title_full Molecular mechanisms of docetaxel resistance in prostate cancer
title_fullStr Molecular mechanisms of docetaxel resistance in prostate cancer
title_full_unstemmed Molecular mechanisms of docetaxel resistance in prostate cancer
title_short Molecular mechanisms of docetaxel resistance in prostate cancer
title_sort molecular mechanisms of docetaxel resistance in prostate cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8992564/
https://www.ncbi.nlm.nih.gov/pubmed/35582222
http://dx.doi.org/10.20517/cdr.2020.37
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