Contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer
An important clinical challenge in prostate cancer therapy is the inevitable transition from androgen-sensitive to castration-resistant and metastatic prostate cancer. Albeit the androgen receptor (AR) signaling axis has been targeted, the biological mechanism underlying the lethal event of androgen...
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BioMed Central
2014
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pubmed-39751762014-04-05 Contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer Li, Ping Yang, Ru Gao, Wei-Qiang Review An important clinical challenge in prostate cancer therapy is the inevitable transition from androgen-sensitive to castration-resistant and metastatic prostate cancer. Albeit the androgen receptor (AR) signaling axis has been targeted, the biological mechanism underlying the lethal event of androgen independence remains unclear. New emerging evidences indicate that epithelial-to-mesenchymal transition (EMT) and cancer stem cells (CSCs) play crucial roles during the development of castration-resistance and metastasis of prostate cancer. Notably, EMT may be a dynamic process. Castration can induce EMT that may enhance the stemness of CSCs, which in turn results in castration-resistance and metastasis. Reverse of EMT may attenuate the stemness of CSCs and inhibit castration-resistance and metastasis. These prospective approaches suggest that therapies target EMT and CSCs may cast a new light on the treatment of castration-resistant prostate cancer (CRPC) in the future. Here we review recent progress of EMT and CSCs in CRPC. BioMed Central 2014-03-12 /pmc/articles/PMC3975176/ /pubmed/24618337 http://dx.doi.org/10.1186/1476-4598-13-55 Text en Copyright © 2014 Li et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Li, Ping Yang, Ru Gao, Wei-Qiang |
spellingShingle |
Li, Ping Yang, Ru Gao, Wei-Qiang Contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer |
author_facet |
Li, Ping Yang, Ru Gao, Wei-Qiang |
author_sort |
Li, Ping |
title |
Contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer |
title_short |
Contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer |
title_full |
Contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer |
title_fullStr |
Contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer |
title_full_unstemmed |
Contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer |
title_sort |
contributions of epithelial-mesenchymal transition and cancer stem cells to the development of castration resistance of prostate cancer |
description |
An important clinical challenge in prostate cancer therapy is the inevitable transition from androgen-sensitive to castration-resistant and metastatic prostate cancer. Albeit the androgen receptor (AR) signaling axis has been targeted, the biological mechanism underlying the lethal event of androgen independence remains unclear. New emerging evidences indicate that epithelial-to-mesenchymal transition (EMT) and cancer stem cells (CSCs) play crucial roles during the development of castration-resistance and metastasis of prostate cancer. Notably, EMT may be a dynamic process. Castration can induce EMT that may enhance the stemness of CSCs, which in turn results in castration-resistance and metastasis. Reverse of EMT may attenuate the stemness of CSCs and inhibit castration-resistance and metastasis. These prospective approaches suggest that therapies target EMT and CSCs may cast a new light on the treatment of castration-resistant prostate cancer (CRPC) in the future. Here we review recent progress of EMT and CSCs in CRPC. |
publisher |
BioMed Central |
publishDate |
2014 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3975176/ |
_version_ |
1612073990847725568 |