Metabolic plasticity in castration-resistant prostate cancer: reprogramming mechanisms and therapeutic opportunities.

Authors

Yanzhi Lou, Zhengda Lou, Luo He, Junfeng Luo

Published in

Cellular signalling. Pages 112885. Sep 12, 2026. Epub Sep 12, 2026.

Abstract

Prostate cancer (PCa) is one of the most common malignant tumors, and most patients develop castration-resistant prostate cancer (CRPC) after androgen deprivation therapy (ADT). Metabolic plasticity, which allows cancer cells to reprogram glucose, lipid, and glutamine utilization, plays a key role. This metabolic adaptation meets the bioenergetic and biosynthetic needs of tumor cells, and it can interact with the androgen receptor (AR) signaling pathway bidirectionally to evade immune surveillance via metabolic reprogramming. Current treatments include single metabolic node inhibition and AR-guided combination therapy. However, due to intratumoral metabolic heterogeneity, compensatory pathway activation, and systemic metabolic toxicity of drugs, there is a need to explore new intervention targets and strategies. This article comprehensively discusses the metabolic network, regulatory mechanism, and current challenges of CRPC in order to provide a theoretical basis for clinical prevention and treatment.

PMID:
42731739
Bibliographic data and abstract were imported from PubMed on 13 Sep 2026.

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