ArticleCell death & disease2024
Targeting valine catabolism to inhibit metabolic reprogramming in prostate cancer.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- MMSDH facilitates ACSL4 propionylation to counteract ferroptosis upon hypoxia and impairs PDAC chemotherapy efficacy.Nature cancer · 2026Article
- Lifelong restriction of dietary valine has sex-specific benefits for health and lifespan in mice.Nature aging · 2026Article
- Isoleucine and valine promote prostate cancer progression via propionyl-CoA-mediated cholesterol metabolism.Nature metabolism · 2026Article
- A fatty acid metabolism-based deep learning model predicts biochemical recurrence and identifies NUDT19 as a candidate metabolic factor in prostate cancer.World journal of surgical oncology · 2026Article
- Amino Acids as Targets for Immunotherapy against Solid Tumors.Cell biochemistry and biophysics · 2026Review
- Causal links of 233 metabolic markers to benign prostatic hyperplasia: Mendelian randomization and RNA-sequencing insights.Journal of the Chinese Medical Association : JCMA · 2026Article
- Targeting NXPH4/ALDH1L2 signaling suppresses enzalutamide resistance in prostate cancer.Cell death discovery · 2026Article
- Branched-chain amino acid transaminases as promising targets in tumor therapy.Frontiers in cell and developmental biology · 2026Review
- Stroma-driven horizontal transfer of TCA-related proteins mediates metabolic plasticity and imatinib resistance in chronic myeloid leukemia.Cell communication and signaling : CCS · 2025Article
- Lifelong restriction of dietary valine has sex-specific benefits for health and lifespan in mice.bioRxiv : the preprint server for biology · 2025Article
- Genome-Scale Metabolic Modeling Identifies Synergistic Metabolites that Enhance 5-Fluorouracil Efficacy in Colon Cancer.Iranian biomedical journal · 2025Article
- Deubiquitination of DNM1L by USP3 triggers the development and metastasis of gallbladder carcinoma.Biology direct · 2025Article
- Metabolomics- and Proteomics-Based Disease Diagnostic Classifier Model for the Prediction and Diagnosis of Colorectal Carcinoma.Journal of proteome research · 2025Article
- Multi-omic insights into mitochondrial dysfunction and prostatic disease: evidence from transcriptomics, proteomics, and methylomics.Frontiers in genetics · 2025Article
- Metabolomic profiling of childhood medulloblastoma: contributions and relevance to diagnosis and molecular subtyping.Journal of cancer research and clinical oncology · 2024Review
- Identification of HIBCH and MGME1 as Mitochondrial Dynamics-Related Biomarkers in Alzheimer's Disease Via Integrated Bioinformatics Analysis.IET systems biologyArticle
- Causal Association Between Gut Microbiota, Plasma Metabolites, and Prostate Cancer: Two-Step Mendelian Randomization Study.Dose-response : a publication of International Hormesis SocietyArticle
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming and energetic rewiring are hallmarks of cancer that fuel disease progression and facilitate therapy evasion. The remodelling of oxidative phosphorylation and enhanced lipogenesis have previously been characterised as key metabolic features of prostate cancer (PCa). Recently, succinate-dependent mitochondrial reprogramming was identified in high-grade prostate tumours, as well as upregulation of the enzymes associated with branched-chain amino acid (BCAA) catabolism. In this study, we hypothesised that the degradation of the BCAAs, particularly valine, may play a critical role in anapleurotic refuelling of the mitochondrial succinate pool, as well as the maintenance of intracellular lipid metabolism. Through the suppression of BCAA availability, we report significantly reduced lipid content, strongly indicating that BCAAs are important lipogenic fuels in PCa. This work also uncovered a novel compensatory mechanism, whereby fatty acid uptake is increased in response to extracellular valine deprivation. Inhibition of valine degradation via suppression of 3-hydroxyisobutyryl-CoA hydrolase (HIBCH) resulted in a selective reduction of malignant prostate cell proliferation, decreased intracellular succinate and impaired cellular respiration. In combination with a comprehensive multi-omic investigation that incorporates next-generation sequencing, metabolomics, and high-content quantitative single-cell imaging, our work highlights a novel therapeutic target for selective inhibition of metabolic reprogramming in PCa.
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