ArticleCell death & disease2025
Prostate cancer exploits BRD9-driven metabolic reprogramming to shape the aggressive phenotype.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Aberrant activation of epigenetic BRD9-DGAT1 axis promotes lipid droplets deposition and ferroptosis resistance in YAP-high prostate cancer.Cell death & disease · 2026Article
- The SWI/SNF complex in tumor metabolism: Mechanisms and therapeutic implications.The Journal of biological chemistry · 2026Review
- Review
- Glyoxalase 2 Drives D-Lactate Oncometabolite Signaling to Promote Prostate Cancer Aggressiveness via FAK/Src Activation.Antioxidants (Basel, Switzerland) · 2026Article
- Exploiting Oxidative Stress as Achilles' Heel: From Redox Homeostasis to Ferroptosis in Prostate Cancer.Antioxidants (Basel, Switzerland) · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
The aggressive phenotype of prostate cancer (PCa) requires adaptation to androgen deprivation (AD) to progress into castration-resistant PCa (CRPC), including adaptation to AD-induced oxidative stress. However, our understanding of the oncogenes that maintain the redox balance during CRPC progression is limited. Here, we identified Bromodomain-containing protein 9 (BRD9) as a metabolic checkpoint for reprogramming cell metabolism to support tumor growth and impart a castration-resistant phenotype under metabolic and oxidative stress. Following oxidation, BRD9 recruited the nuclear transcription factor-Y A-subunit (NFYA) to induce glycogen phosphorylase L (PYGL) expression, which directed glucose utilization through the pentose phosphate pathway, generating NADPH, and promoting clearance of reactive oxygen species (ROS), thus maintaining redox balance. By disturbing redox homeostasis, BRD9 inhibition exerted oxidative pressure on PCa cells, sensitizing them to radiotherapy. This work identified BRD9 as a novel component in antioxidant reprogramming and indicates BRD9 targeting as a promising treatment strategy for PCa therapy.
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Registered trials
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