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Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells

Androgen/androgen receptor (AR) signaling is a significant driver of prostate cancer progression, therefore androgen-deprivation therapy (ADT) is often used as a standard form of treatment for advanced and metastatic prostate cancer patients. However, after several years of ADT, prostate cancer prog...

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Detalles Bibliográficos
Autores principales: Izumi, Kouji, Mizokami, Atsushi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6463189/
https://www.ncbi.nlm.nih.gov/pubmed/30871130
http://dx.doi.org/10.3390/jcm8030354
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author Izumi, Kouji
Mizokami, Atsushi
author_facet Izumi, Kouji
Mizokami, Atsushi
author_sort Izumi, Kouji
collection PubMed
description Androgen/androgen receptor (AR) signaling is a significant driver of prostate cancer progression, therefore androgen-deprivation therapy (ADT) is often used as a standard form of treatment for advanced and metastatic prostate cancer patients. However, after several years of ADT, prostate cancer progresses to castration-resistant prostate cancer (CRPC). Androgen/AR signaling is still considered an important factor for prostate cancer cell survival following CRPC progression, while recent studies have reported dichotomic roles for androgen/AR signaling. Androgen/AR signaling increases prostate cancer cell proliferation, while simultaneously inhibiting migration. As a result, ADT can induce prostate cancer metastasis. Several C-C motif ligand (CCL)-receptor (CCR) axes are involved in cancer cell migration related to blockade of androgen/AR signaling. The CCL2-CCR2 axis is negatively regulated by androgen/AR signaling, with the CCL22-CCR4 axis acting as a further downstream mediator, both of which promote prostate cancer cell migration. Furthermore, the CCL5-CCR5 axis inhibits androgen/AR signaling as an upstream mediator. CCL4 is involved in prostate carcinogenesis through macrophage AR signaling, while the CCL21-CCR7 axis in prostate cancer cells is activated by tumor necrotic factor, which is secreted when androgen/AR signaling is inhibited. Finally, the CCL2-CCR2 axis has recently been demonstrated to be a key contributor to cabazitaxel resistance in CRPC.
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spelling pubmed-64631892019-04-19 Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells Izumi, Kouji Mizokami, Atsushi J Clin Med Review Androgen/androgen receptor (AR) signaling is a significant driver of prostate cancer progression, therefore androgen-deprivation therapy (ADT) is often used as a standard form of treatment for advanced and metastatic prostate cancer patients. However, after several years of ADT, prostate cancer progresses to castration-resistant prostate cancer (CRPC). Androgen/AR signaling is still considered an important factor for prostate cancer cell survival following CRPC progression, while recent studies have reported dichotomic roles for androgen/AR signaling. Androgen/AR signaling increases prostate cancer cell proliferation, while simultaneously inhibiting migration. As a result, ADT can induce prostate cancer metastasis. Several C-C motif ligand (CCL)-receptor (CCR) axes are involved in cancer cell migration related to blockade of androgen/AR signaling. The CCL2-CCR2 axis is negatively regulated by androgen/AR signaling, with the CCL22-CCR4 axis acting as a further downstream mediator, both of which promote prostate cancer cell migration. Furthermore, the CCL5-CCR5 axis inhibits androgen/AR signaling as an upstream mediator. CCL4 is involved in prostate carcinogenesis through macrophage AR signaling, while the CCL21-CCR7 axis in prostate cancer cells is activated by tumor necrotic factor, which is secreted when androgen/AR signaling is inhibited. Finally, the CCL2-CCR2 axis has recently been demonstrated to be a key contributor to cabazitaxel resistance in CRPC. MDPI 2019-03-13 /pmc/articles/PMC6463189/ /pubmed/30871130 http://dx.doi.org/10.3390/jcm8030354 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Izumi, Kouji
Mizokami, Atsushi
Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells
title Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells
title_full Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells
title_fullStr Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells
title_full_unstemmed Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells
title_short Suppressive Role of Androgen/Androgen Receptor Signaling via Chemokines on Prostate Cancer Cells
title_sort suppressive role of androgen/androgen receptor signaling via chemokines on prostate cancer cells
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6463189/
https://www.ncbi.nlm.nih.gov/pubmed/30871130
http://dx.doi.org/10.3390/jcm8030354
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