ArticleCancers2020
ATP Production Relies on Fatty Acid Oxidation Rather than Glycolysis in Pancreatic Ductal Adenocarcinoma.
Article in Cancers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 58 citations in OpenAlex.
- Fingerprinting the Metabolic and Lipidomic Landscapes of Pancreatic Ductal Adenocarcinoma with MALDI Imaging.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Inhibiting Fatty Acid Oxidation Reverses Autophagy-Mediated Acquired Chemotherapy Resistance in Pancreatic Ductal Adenocarcinoma.Cancer research · 2026Article
- Metabolic plasticity in pancreatic ductal adenocarcinoma progression and response to treatment.Molecular cancer · 2026Review
- Substituting Soybean Meal With Rapeseed Green Cake: A Holistic Assessment of Growth, Metabolic Response, and Intestinal Status in Juvenile Largemouth Bass (Aquaculture nutrition · 2026Article
- Surgery-Induced Neutrophil Extracellular Traps Promote Tumor Metastasis by Reprogramming Cancer Cell Lipid Metabolism.Cancer research · 2025Article
- SLC25A11 Is Associated with KDM2A-Dependent Reduction in rRNA Transcription Induced by Aminooxyacetic Acid.Cells · 2025Article
- Serum carnitine and cancer risk: a Mendelian randomization study identifying pancreatic cancer as a modifiable metabolic target.Discover oncology · 2025Article
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- The mechanisms and clinical significance of CD8Cancer biology & medicine · 2025Review
- G-protein coupled receptors in metabolic reprogramming and cancer.Pharmacology & therapeutics · 2025Review
- N-phenylmaleimide induces bioenergetic switch and suppresses tumor growth in glioblastoma tumorspheres by inhibiting SLC25A11.Cancer cell international · 2025Article
- Impaired mitochondrial integrity and compromised energy production underscore the mechanism underlying CoASY protein-associated neurodegeneration.Cellular and molecular life sciences : CMLS · 2025Article
- Deciphering molecular crosstalk mechanisms between skeletal muscle atrophy and KRAS-mutant pancreatic cancer: a literature review.Hepatobiliary surgery and nutrition · 2025Review
- Global research trends and emerging themes in osteosarcoma metabolomics: a bibliometric and visualization analysis.Frontiers in molecular biosciences · 2025Article
- GSTP1 knockdown induces metabolic changes affecting energy production and lipid balance in pancreatic cancer cells.Molecular & cellular oncology · 2025Article
- Elucidating the protective mechanisms of umbilical cord mesenchymal stem cells against stenosis-induced deep venous thrombosis during pregnancy: a transcriptomic and metabolomic study.Frontiers in cell and developmental biology · 2025Article
- Theoretical Modeling of the Interactions of CoFeCurrent medicinal chemistry · 2025Article
- Loss ofTheranostics · 2025Article
- Fatty Acid Synthase (FASN) Inhibitors Suppress Metformin-Induced Fat Accumulation and Apoptosis in H4IIE Hepatocellular Carcinoma Cells.Development & reproduction · 2024Article
- Genetically predicted gut bacteria, circulating bacteria-associated metabolites and pancreatic ductal adenocarcinoma: a Mendelian randomisation study.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Glycolysis is known as the main pathway for ATP production in cancer cells. However, in cancer cells, glucose deprivation for 24 h does not reduce ATP levels, whereas it does suppress lactate production. In this study, metabolic pathways were blocked to identify the main pathway of ATP production in pancreatic ductal adenocarcinoma (PDAC). Blocking fatty acid oxidation (FAO) decreased ATP production by 40% in cancer cells with no effect on normal cells. The effects of calorie balanced high- or low-fat diets were tested to determine whether cancer growth is modulated by fatty acids instead of calories. A low-fat diet caused a 70% decrease in pancreatic preneoplastic lesions compared with the control, whereas a high-fat diet caused a two-fold increase in preneoplastic lesions accompanied with increase of ATP production in the Kras (G12D)/Pdx1-cre PDAC model. The present results suggest that ATP production in cancer cells is dependent on FAO rather than on glycolysis, which can be a therapeutic approach by targeting cancer energy metabolism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.