ArticleCancer discovery2021
Medium-Chain Acyl-CoA Dehydrogenase Protects Mitochondria from Lipid Peroxidation in Glioblastoma.
Article in Cancer discovery, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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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
37 citing papers in PubMed, 57 citations in OpenAlex.
- PPARγ Signaling in the Central Nervous System: A Review of the Implications in Synaptic Plasticity, Neuroinflammatory and Neoplastic Processes.Neurochemical research · 2026Review
- Mitochondrial Metabolic Reprogramming in Glioma: Mechanisms of Tumorigenesis and Implications for Clinical Therapy.CNS neuroscience & therapeutics · 2026Review
- Fatty Acid Metabolism Rewires Glioblastoma Progression and Treg-Mediated Immune Resistance.Cancers · 2026Review
- In Vivo ORF Overexpression Screening Identifies CCN4 as a Regulator of Glioblastoma Growth Validated Across Multiple Models.International journal of molecular sciences · 2026Article
- Plasma metabolomic profiling identifies a metabolic signature for non-muscle-invasive bladder cancer independent of hematuria.Biology direct · 2026Article
- Ferroptosis and metabolic reprogramming in the immunosuppressive microenvironment of glioblastoma: emerging mechanisms and novel strategies.Frontiers in immunology · 2026Review
- Exploring the diagnostic and prognostic potential of LCFAs' metabolic and biosynthetic pathways in glioblastoma multiforme using a bioinformatics approach.Research in pharmaceutical sciences · 2025Article
- Extracellular Vesicles as Novel Biomarkers for Tumor Association in Intermediate-Risk Paraneoplastic Neurologic Syndromes.Neurology(R) neuroimmunology & neuroinflammation · 2025Observational
- Harnessing ferroptosis to transform glioblastoma therapy and surmount treatment resistance.Cell death discovery · 2025Review
- [Down-regulation of ACADM-mediated lipotoxicity inhibits invasion and metastasis of estrogen receptor-positive breast cancer cells].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025Article
- Metabolic traits shape responses to LSD1-directed therapy in glioblastoma tumor-initiating cells.Science advances · 2025Article
- CPT1A/HIF-1α positive feedback loop induced fatty acid oxidation metabolic pathway contributes to the L-ascorbic acid-driven angiogenesis in breast cancer.Breast cancer research : BCR · 2025Article
- Metabolic Reprogramming of Gastric Cancer Revealed by a Liquid Chromatography-Mass Spectrometry-Based Metabolomics Study.Metabolites · 2025Article
- TRAF3 loss protects glioblastoma cells from lipid peroxidation and immune elimination via dysregulated lipid metabolism.The Journal of clinical investigation · 2025Article
- Metabolism: an important player in glioma survival and development.Discover oncology · 2024Review
- A cell state-specific metabolic vulnerability to GPX4-dependent ferroptosis in glioblastoma.The EMBO journal · 2024Article
- Dexamethasone Impairs ATP Production and Mitochondrial Performance in Human Trabecular Meshwork Cells.Current issues in molecular biology · 2024Article
- Association of total bilirubin and prognosis in disorders of consciousness.Scientific reports · 2024Article
- Combined Multi-Omics Analysis Reveals the Potential Role ofInternational journal of molecular sciences · 2024Article
- Metabolic Plasticity of Glioblastoma Cells in Response to DHODH Inhibitor BAY2402234 Treatment.Metabolites · 2024Article
Corrections and comments
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Authors and funding
29 authors at 3 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is highly resistant to chemotherapies, immune-based therapies, and targeted inhibitors. To identify novel drug targets, we screened orthotopically implanted, patient-derived glioblastoma sphere-forming cells using an RNAi library to probe essential tumor cell metabolic programs. This identified high dependence on mitochondrial fatty acid metabolism. We focused on medium-chain acyl-CoA dehydrogenase (MCAD), which oxidizes medium-chain fatty acids (MCFA), due to its consistently high score and high expression among models and upregulation in GBM compared with normal brain. Beyond the expected energetics impairment, MCAD depletion in primary GBM models induced an irreversible cascade of detrimental metabolic effects characterized by accumulation of unmetabolized MCFAs, which induced lipid peroxidation and oxidative stress, irreversible mitochondrial damage, and apoptosis. Our data uncover a novel protective role for MCAD to clear lipid molecules that may cause lethal cell damage, suggesting that therapeutic targeting of MCFA catabolism may exploit a key metabolic feature of GBM. SIGNIFICANCE: MCAD exerts a protective role to prevent accumulation of toxic metabolic by-products in glioma cells, actively catabolizing lipid species that would otherwise affect mitochondrial integrity and induce cell death. This work represents a first demonstration of a nonenergetic role for dependence on fatty acid metabolism in cancer.
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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.