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Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment

High levels of chemokine (C-C motif) ligand 2 (CCL2) promote the metastatic dissemination of prostate cancer by recruiting macrophages to neoplastic lesions. We have recently discovered that inhibiting the androgen receptor (AR) in prostate cancer cells or tumor-infiltrating macrophages results in t...

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Detalles Bibliográficos
Autores principales: Lin, Wen-Jye, Izumi, Kouji
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203538/
https://www.ncbi.nlm.nih.gov/pubmed/25339999
http://dx.doi.org/10.4161/onci.27871
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author Lin, Wen-Jye
Izumi, Kouji
author_facet Lin, Wen-Jye
Izumi, Kouji
author_sort Lin, Wen-Jye
collection PubMed
description High levels of chemokine (C-C motif) ligand 2 (CCL2) promote the metastatic dissemination of prostate cancer by recruiting macrophages to neoplastic lesions. We have recently discovered that inhibiting the androgen receptor (AR) in prostate cancer cells or tumor-infiltrating macrophages results in the upregulation CCL2 and promotes disease progression by activating signal transducer and activator of transcription 3 (STAT3) and by favoring the epithelial-to-mesenchymal transition. Our results indicate that the sole inhibition of AR as a therapeutic intervention against prostate cancer is intrinsically destined to failed.
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spelling pubmed-42035382015-02-14 Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment Lin, Wen-Jye Izumi, Kouji Oncoimmunology Author's View High levels of chemokine (C-C motif) ligand 2 (CCL2) promote the metastatic dissemination of prostate cancer by recruiting macrophages to neoplastic lesions. We have recently discovered that inhibiting the androgen receptor (AR) in prostate cancer cells or tumor-infiltrating macrophages results in the upregulation CCL2 and promotes disease progression by activating signal transducer and activator of transcription 3 (STAT3) and by favoring the epithelial-to-mesenchymal transition. Our results indicate that the sole inhibition of AR as a therapeutic intervention against prostate cancer is intrinsically destined to failed. Landes Bioscience 2014-02-14 /pmc/articles/PMC4203538/ /pubmed/25339999 http://dx.doi.org/10.4161/onci.27871 Text en Copyright © 2014 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Author's View
Lin, Wen-Jye
Izumi, Kouji
Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment
title Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment
title_full Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment
title_fullStr Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment
title_full_unstemmed Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment
title_short Androgen receptor, ccl2, and epithelial-mesenchymal transition: A dangerous affair in the tumor microenvironment
title_sort androgen receptor, ccl2, and epithelial-mesenchymal transition: a dangerous affair in the tumor microenvironment
topic Author's View
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4203538/
https://www.ncbi.nlm.nih.gov/pubmed/25339999
http://dx.doi.org/10.4161/onci.27871
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