ArticleThe Prostate2022
Prostate cancer cells demonstrate unique metabolism and substrate adaptability acutely after androgen deprivation therapy.
Article in The Prostate, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- Dysregulation of the urea cycle - potential targets for treatment and diagnosis in prostate cancer.Expert reviews in molecular medicine · 2026Review
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- Association between duration of neoadjuvant hormonal therapy and prostate-specific antigen response and pathological outcomes in high-risk prostate cancer undergoing robot-assisted radical prostatectomy.Frontiers in oncology · 2026Article
- Research on the potential mechanisms and therapeutic drug for the co-occurrence of major depressive disorder in castration-resistant prostate cancer.Scientific reports · 2025Article
- Beta-blockers prolong response to androgen deprivation therapy in prostate cancer through modulation of the neuro-immuno-oncology axis.Journal of translational medicine · 2025Article
- Toad venom-derived bufadienolides and their therapeutic application in prostate cancers: Current status and future directions.Frontiers in chemistry · 2023Review
- Prostate cancer cells demonstrate unique metabolism and substrate adaptability acutely after androgen deprivation therapy.The Prostate · 2022Article
- Androgen Metabolism and Response in Prostate Cancer Anti-Androgen Therapy Resistance.International journal of molecular sciences · 2022Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundAndrogen deprivation therapy (ADT) has been the standard of care for advanced hormone-sensitive prostate cancer (PC), yet tumors invariably develop resistance resulting in castrate-resistant PC. The acute response of cancer cells to ADT includes apoptosis and cell death, but a large fraction remains arrested but viable. In this study, we focused on intensively characterizing the early metabolic changes that result after ADT to define potential metabolic targets for treatment.
methodsA combination of mass spectrometry, optical metabolic imaging which noninvasively measures drug responses in cells, oxygen consumption rate, and protein expression analysis was used to characterize and block metabolic pathways over several days in multiple PC cell lines with variable hormone response status including ADT sensitive lines LNCaP and VCaP, and resistant C4-2 and DU145.
resultsMass spectrometry analysis of LNCaP pre- and postexposure to ADT revealed an abundance of glycolytic intermediates after ADT. In LNCaP and VCaP, a reduction in the optical redox ratio [NAD(P)H/FAD], extracellular acidification rate, and a downregulation of key regulatory enzymes for fatty acid and glutamine utilization was acutely observed after ADT. Screening several metabolic inhibitors revealed that blocking fatty acid oxidation and synthesis reversed this stress response in the optical redox ratio seen with ADT alone in LNCaP and VCaP. In contrast, both cell lines demonstrated increased sensitivity to the glycolytic inhibitor 2-Deoxy- d-glucose(2-DG) and maintained sensitivity to electron transport chain inhibitor Malonate after ADT exposure. ADT followed by 2-DG results in synergistic cell death, a result not seen with simultaneous administration.
conclusionsHormone-sensitive PC cells displayed altered metabolic profiles early after ADT including an overall depression in energy metabolism, induction of a quiescent/senescent phenotype, and sensitivity to selected metabolic inhibitors. Glycolytic blocking agents (e.g., 2-DG) as a sequential treatment after ADT may be promising.
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