Abstract
There is an urgent need for exploring new actionable targets other than androgen receptor to improve outcome from lethal castration-resistant prostate cancer. Tumor metabolism has reemerged as a hallmark of cancer that drives and supports oncogenesis. In this regard, it is important to understand the relationship between distinctive metabolic features, androgen receptor signaling, genetic drivers in prostate cancer, and the tumor microenvironment (symbiotic and competitive metabolic interactions) to identify metabolic vulnerabilities. We explore the links between metabolism and gene regulation, and thus the unique metabolic signatures that define the malignant phenotypes at given stages of prostate tumor progression. We also provide an overview of current metabolism-based pharmacological strategies to be developed or repurposed for metabolism-based therapeutics for castration-resistant prostate cancer.
Funder
NCI
U.S. Department of Defense Prostate Cancer Research Program
U.S. Department of Defense
Institute for Prostate Cancer Research at the University of Washington and Fred Hutchinson Cancer Research Center
Canadian Institutes of Health Research
Mitacs Accelerate Program
Prostate Cancer Foundation—British Columbia (PCFBC) Grant-in-Aid
VA merit review award
Weill Cornell Medicine SPORE in Prostate Cancer
Subject
Molecular Biology,Biochemistry
Cited by
6 articles.
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