ArticleCell death & disease2025
TXNIP upregulation controls metabolism and cell cycle during androgen deprivation therapy in prostate cancer.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Thioredoxin-Interacting Protein (TXNIP) is an arrestin at the crossroad of redox and glycolytic metabolisms. Prostate cancer (PCa) exhibits a unique metabolic profile due to the glycolytic nature of healthy prostate tissue. We hypothesize that TXNIP plays a pivotal role in the progression of PCa to castration-resistant prostate cancer (CRPC), an incurable stage of the disease characterized by profound metabolic reprogramming and independence from androgens. Only a subset of patients progresses to CRPC, and current stratification tools lack robust biomarkers. TXNIP expression is directly suppressed by androgens and diminishes during tumor initiation and progression, as demonstrated in both human samples and a prostate adenocarcinoma mouse model (TRAMP). TXNIP regulates glucose metabolism by sequestering the glucose transporter GLUT1 away from the membrane, shifting metabolism from glycolysis to glutaminolysis. Nuclear-localized TXNIP induces cell cycle arrest through the upregulation of p27
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