ArticleBritish journal of cancer2020
MYC regulates fatty acid metabolism through a multigenic program in claudin-low triple negative breast cancer.
Article in British journal of cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 82 citations in OpenAlex.
- Detachment-Induced FAK-STAT3-NNMT Inhibits CTCs Anoikis to Promote Breast Cancer Metastasis by Enhancing Fatty Acid Oxidation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Metabolic permissiveness: how tissue context shapes cancer.Genes & development · 2026Review
- Fatty Acid Synthase as a Potential Metabolic Vulnerability in Ocular Adnexal Sebaceous Carcinoma.Cancers · 2026Article
- Isoliquiritigenin Suppresses Oral Squamous Cell Carcinoma Progression by Targeting FABP5-Mediated Lipid Metabolism: Association with the circPOLB/miR-548ae-3p/C-MYC Axis.Oncology research · 2026Article
- Surgery-Induced Neutrophil Extracellular Traps Promote Tumor Metastasis by Reprogramming Cancer Cell Lipid Metabolism.Cancer research · 2025Article
- Lipolysis gone rogue: the HSL connection in feeding cancer.Cell biology and toxicology · 2025Review
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- Lipid metabolic reprograming: the unsung hero in breast cancer progression and tumor microenvironment.Molecular cancer · 2025Review
- CD36 as a Therapeutic Target in Tumor Microenvironment and Lipid Metabolism.Anti-cancer agents in medicinal chemistry · 2025Review
- Fueling the fire-a pan-cancer analysis of MYC-regulated lipid metabolism.Frontiers in cell and developmental biology · 2025Review
- Fibroblast Growth Factor Receptor 4 Promotes Triple-Negative Breast Cancer Progression via Regulating Fatty Acid Metabolism Through the AKT/RYR2 Signaling.Cancer medicine · 2024Article
- IGFBP1 promotes the proliferation and migration of lung adenocarcinoma cells through the PPARα pathway.Translational oncology · 2024Article
- Reciprocal interactions between lncRNAs and MYC in colorectal cancer: partners in crime.Cell death & disease · 2024Review
- MYC Oncogene: A Druggable Target for Treating Cancers with Natural Products.Aging and disease · 2024Review
- Metabolite profiles of medulloblastoma for rapid and non-invasive detection of molecular disease groups.EBioMedicine · 2024Article
- SERPINB3-MYC axis induces the basal-like/squamous subtype and enhances disease progression in pancreatic cancer.Cell reports · 2023Article
- Review
- Integrative multi-omic sequencing reveals the MMTV-Myc mouse model mimics human breast cancer heterogeneity.Breast cancer research : BCR · 2023Article
- Acetate acts as a metabolic immunomodulator by bolstering T-cell effector function and potentiating antitumor immunity in breast cancer.Nature cancer · 2023Article
- Unlocking Translational Potential: Conditionally Reprogrammed Cells in Advancing Breast Cancer Research.Cells · 2023Review
Corrections and comments
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Authors and funding
23 authors at 7 institutions in 3 countries.
Funding
Abstract
backgroundRecent studies have suggested that fatty acid oxidation (FAO) is a key metabolic pathway for the growth of triple negative breast cancers (TNBCs), particularly those that have high expression of MYC. However, the underlying mechanism by which MYC promotes FAO remains poorly understood.
methodsWe used a combination of metabolomics, transcriptomics, bioinformatics, and microscopy to elucidate a potential mechanism by which MYC regulates FAO in TNBC.
resultsWe propose that MYC induces a multigenic program that involves changes in intracellular calcium signalling and fatty acid metabolism. We determined key roles for fatty acid transporters (CD36), lipases (LPL), and kinases (PDGFRB, CAMKK2, and AMPK) that each contribute to promoting FAO in human mammary epithelial cells that express oncogenic levels of MYC. Bioinformatic analysis further showed that this multigenic program is highly expressed and predicts poor survival in the claudin-low molecular subtype of TNBC, but not other subtypes of TNBCs, suggesting that efforts to target FAO in the clinic may best serve claudin-low TNBC patients.
conclusionWe identified critical pieces of the FAO machinery that have the potential to be targeted for improved treatment of patients with TNBC, especially the claudin-low molecular subtype.
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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.