ArticleScience advances2021
Fatty acid oxidation is a druggable gateway regulating cellular plasticity for driving metastasis in breast cancer.
Article in Science advances, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
62 citing papers in PubMed.
- Mitochondrial dynamics: A promising tool for personalized TNBC management.Genes & diseases · 2026Review
- Bidirectional Feedback Between Metabolic Reprogramming and Epithelial-Mesenchymal Transition: From Mechanisms to Therapeutic Interventions.Molecules (Basel, Switzerland) · 2026Review
- Genome-wide chromatin profiling reveals a nonlimiting role for RXR in macrophage-like cells stimulated with multiple nuclear receptor agonists.The Journal of biological chemistry · 2026Article
- Mechanisms of fatty acid metabolism in tumor metastasis and targeted therapeutic strategies.Discover oncology · 2026Review
- The crosstalk between epigenetics and metabolism in the malignant cell.Discover oncology · 2026Review
- Subtype-Stratified Consensus Gene Signatures: Bridging Tumor Cell Biology, Immune Microenvironment, and Clinical Prognosis in Breast Cancer.International journal of molecular sciences · 2026Article
- Large adipocytes increase vesicle-mediated lipid release and promote breast cancer malignancy.Cell reports · 2026Article
- Phase separation of DDHD2 remodels lipid metabolism to dictate treatment sensitivity in luminal breast cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- CPT1A as a metabolic gatekeeper linking fatty acid oxidation, ferroptosis resistance, and breast cancer stemness.Frontiers in oncology · 2026Review
- Metabolic adaptations in cancer progression.Physiological reviews · 2026Review
- Introduction to Cancer Metabolism.Cancer treatment and research · 2026Review
- Evaluating the potential causal relationship between carnitine-related metabolites and breast cancer: a Mendelian randomization and transcriptomic analysis.Archives of medical science : AMS · 2026Article
- Stroma-driven horizontal transfer of TCA-related proteins mediates metabolic plasticity and imatinib resistance in chronic myeloid leukemia.Cell communication and signaling : CCS · 2025Article
- Implantation of engineered adipocytes suppresses tumor progression in cancer models.Nature biotechnology · 2025Article
- NPR1 Promotes Lipid Droplet Lipolysis to Enhance Mitochondrial Oxidative Phosphorylation and Fuel Gastric Cancer Metastasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Large adipocytes alter mode of lipid release and promote breast cancer malignancy.bioRxiv : the preprint server for biology · 2025Article
- SENP1: A perspective from immune cells to disease (Review).Oncology reports · 2025Review
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- G-protein coupled receptors in metabolic reprogramming and cancer.Pharmacology & therapeutics · 2025Review
- Lipid metabolic reprograming: the unsung hero in breast cancer progression and tumor microenvironment.Molecular cancer · 2025Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
33 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell state transitions control the functional behavior of cancer cells. Epithelial-to-mesenchymal transition (EMT) confers cancer stem cell-like properties, enhanced tumorigenicity and drug resistance to tumor cells, while mesenchymal-epithelial transition (MET) reverses these phenotypes. Using high-throughput chemical library screens, retinoids are found to be potent promoters of MET that inhibit tumorigenicity in basal-like breast cancer. Cell state transitions are defined by reprogramming of lipid metabolism. Retinoids bind cognate nuclear receptors, which target lipid metabolism genes, thereby redirecting fatty acids for β-oxidation in the mesenchymal cell state towards lipid storage in the epithelial cell state. Disruptions of key metabolic enzymes mediating this flux inhibit MET. Conversely, perturbations to fatty acid oxidation (FAO) rechannel fatty acid flux and promote a more epithelial cell phenotype, blocking EMT-driven breast cancer metastasis in animal models. FAO impinges on the epigenetic control of EMT through acetyl-CoA-dependent regulation of histone acetylation on EMT genes, thus determining cell states.
Identifiers
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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.