Targeting Inflammatory Signaling in Prostate Cancer Castration Resistance.
Shangwei ZhongChanghao HuangZhikang ChenZihua ChenJun-Li LuoPublished in: Journal of clinical medicine (2021)
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.
Keyphrases
- induced apoptosis
- prostate cancer
- cell cycle arrest
- oxidative stress
- endoplasmic reticulum stress
- cell death
- artificial intelligence
- radical prostatectomy
- squamous cell carcinoma
- signaling pathway
- radiation therapy
- drug delivery
- mesenchymal stem cells
- pi k akt
- rectal cancer
- diabetic rats
- smoking cessation
- cell therapy
- combination therapy