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Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9(®) to better battle prostate cancer progression

Inflammatory cytokines and chemokines released by macrophages in the prostate cancer microenvironment may signal via the androgen receptor (AR) to influence tumor progression. In particular, macrophages appear to promote tumorigenesis by altering the chemokine (C-C motif) ligand 4 (CCL4)/AR signalin...

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Detalles Bibliográficos
Autores principales: Izumi, Kouji, Chang, Chawnshang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902114/
https://www.ncbi.nlm.nih.gov/pubmed/24498558
http://dx.doi.org/10.4161/onci.26853
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author Izumi, Kouji
Chang, Chawnshang
author_facet Izumi, Kouji
Chang, Chawnshang
author_sort Izumi, Kouji
collection PubMed
description Inflammatory cytokines and chemokines released by macrophages in the prostate cancer microenvironment may signal via the androgen receptor (AR) to influence tumor progression. In particular, macrophages appear to promote tumorigenesis by altering the chemokine (C-C motif) ligand 4 (CCL4)/AR signaling axis. This process can be blocked by ASC-J9(®), an enhancer of AR degradation. ASC-J9(®) also inhibits the CCL2-dependent, signal transducer and activator of transcription 3 (STAT3)-mediated pro-metastatic signaling cascade that is generally activated by androgen deprivation therapy. Thus, targeting inflammatory cytokines signaling via the AR, with ASC-J9(®), represents a promising therapeutic approach against prostate cancer progression.
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spelling pubmed-39021142014-02-04 Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9(®) to better battle prostate cancer progression Izumi, Kouji Chang, Chawnshang Oncoimmunology Author's View Inflammatory cytokines and chemokines released by macrophages in the prostate cancer microenvironment may signal via the androgen receptor (AR) to influence tumor progression. In particular, macrophages appear to promote tumorigenesis by altering the chemokine (C-C motif) ligand 4 (CCL4)/AR signaling axis. This process can be blocked by ASC-J9(®), an enhancer of AR degradation. ASC-J9(®) also inhibits the CCL2-dependent, signal transducer and activator of transcription 3 (STAT3)-mediated pro-metastatic signaling cascade that is generally activated by androgen deprivation therapy. Thus, targeting inflammatory cytokines signaling via the AR, with ASC-J9(®), represents a promising therapeutic approach against prostate cancer progression. Landes Bioscience 2013-12-01 2013-10-22 /pmc/articles/PMC3902114/ /pubmed/24498558 http://dx.doi.org/10.4161/onci.26853 Text en Copyright © 2013 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
Izumi, Kouji
Chang, Chawnshang
Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9(®) to better battle prostate cancer progression
title Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9(®) to better battle prostate cancer progression
title_full Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9(®) to better battle prostate cancer progression
title_fullStr Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9(®) to better battle prostate cancer progression
title_full_unstemmed Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9(®) to better battle prostate cancer progression
title_short Targeting inflammatory cytokines-androgen receptor (AR) signaling with ASC-J9(®) to better battle prostate cancer progression
title_sort targeting inflammatory cytokines-androgen receptor (ar) signaling with asc-j9(®) to better battle prostate cancer progression
topic Author's View
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3902114/
https://www.ncbi.nlm.nih.gov/pubmed/24498558
http://dx.doi.org/10.4161/onci.26853
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