Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance

Although castration-resistant prostate cancer (CRPC) as a whole, by its name, refers to the tumors that relapse and/or regrow independently of androgen after androgen deprivation therapy (ADT), untreated tumor, even in early-stage primary prostate cancer (PCa), contains androgen-independent (AI) PCa...

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Autores principales:	Shangwei Zhong, Changhao Huang, Zhikang Chen, Zihua Chen, Jun-Li Luo
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	androgen deprivation therapy (ADT) castration-resistant prostate cancer (CRPC) inflammatory signaling nuclear factor-kappa B (NF-κB) IκB kinase (IKK) macrophage Medicine R
Acceso en línea:	https://doaj.org/article/6d80489b6ba0470e90a9af36efd096d1
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spelling	oai:doaj.org-article:6d80489b6ba0470e90a9af36efd096d12021-11-11T17:38:04ZTargeting Inflammatory Signaling in Prostate Cancer Castration Resistance10.3390/jcm102150002077-0383https://doaj.org/article/6d80489b6ba0470e90a9af36efd096d12021-10-01T00:00:00Zhttps://www.mdpi.com/2077-0383/10/21/5000https://doaj.org/toc/2077-0383Although castration-resistant prostate cancer (CRPC) as a whole, by its name, refers to the tumors that relapse and/or regrow independently of androgen after androgen deprivation therapy (ADT), untreated tumor, even in early-stage primary prostate cancer (PCa), contains androgen-independent (AI) PCa cells. The transformation of androgen-dependent (AD) PCa to AI PCa under ADT is a forced evolutionary process, in which the small group of AI PCa cells that exist in primary tumors has the unique opportunity to proliferate and expand selectively and dominantly, while some AD PCa cells that have escaped from ADT-induced death acquire the capability to survive in an androgen-depleted environment. The adaptation and reprogramming of both PCa cells and the tumor microenvironment (TME) under ADT make PCa much stronger than primary tumors so that, currently, there are no effective therapeutic methods available for the treatment of CRPC. Many mechanisms have been found to be related to the emergence and maintenance of PCa castration resistance; in this review, we focus on the role of inflammatory signaling in both PCa cells and the TME for the emergence and maintenance of CRPC and summarize the recent advances of therapeutic strategies that target inflammatory signaling for the treatment of CRPC.Shangwei ZhongChanghao HuangZhikang ChenZihua ChenJun-Li LuoMDPI AGarticleandrogen deprivation therapy (ADT)castration-resistant prostate cancer (CRPC)inflammatory signalingnuclear factor-kappa B (NF-κB)IκB kinase (IKK)macrophageMedicineRENJournal of Clinical Medicine, Vol 10, Iss 5000, p 5000 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	androgen deprivation therapy (ADT) castration-resistant prostate cancer (CRPC) inflammatory signaling nuclear factor-kappa B (NF-κB) IκB kinase (IKK) macrophage Medicine R
spellingShingle	androgen deprivation therapy (ADT) castration-resistant prostate cancer (CRPC) inflammatory signaling nuclear factor-kappa B (NF-κB) IκB kinase (IKK) macrophage Medicine R Shangwei Zhong Changhao Huang Zhikang Chen Zihua Chen Jun-Li Luo Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance
description	Although castration-resistant prostate cancer (CRPC) as a whole, by its name, refers to the tumors that relapse and/or regrow independently of androgen after androgen deprivation therapy (ADT), untreated tumor, even in early-stage primary prostate cancer (PCa), contains androgen-independent (AI) PCa cells. The transformation of androgen-dependent (AD) PCa to AI PCa under ADT is a forced evolutionary process, in which the small group of AI PCa cells that exist in primary tumors has the unique opportunity to proliferate and expand selectively and dominantly, while some AD PCa cells that have escaped from ADT-induced death acquire the capability to survive in an androgen-depleted environment. The adaptation and reprogramming of both PCa cells and the tumor microenvironment (TME) under ADT make PCa much stronger than primary tumors so that, currently, there are no effective therapeutic methods available for the treatment of CRPC. Many mechanisms have been found to be related to the emergence and maintenance of PCa castration resistance; in this review, we focus on the role of inflammatory signaling in both PCa cells and the TME for the emergence and maintenance of CRPC and summarize the recent advances of therapeutic strategies that target inflammatory signaling for the treatment of CRPC.
format	article
author	Shangwei Zhong Changhao Huang Zhikang Chen Zihua Chen Jun-Li Luo
author_facet	Shangwei Zhong Changhao Huang Zhikang Chen Zihua Chen Jun-Li Luo
author_sort	Shangwei Zhong
title	Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance
title_short	Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance
title_full	Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance
title_fullStr	Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance
title_full_unstemmed	Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance
title_sort	targeting inflammatory signaling in prostate cancer castration resistance
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/6d80489b6ba0470e90a9af36efd096d1
work_keys_str_mv	AT shangweizhong targetinginflammatorysignalinginprostatecancercastrationresistance AT changhaohuang targetinginflammatorysignalinginprostatecancercastrationresistance AT zhikangchen targetinginflammatorysignalinginprostatecancercastrationresistance AT zihuachen targetinginflammatorysignalinginprostatecancercastrationresistance AT junliluo targetinginflammatorysignalinginprostatecancercastrationresistance
_version_	1718432068260593664

Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance

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