ArticleMetabolic engineering2017
Quantitative metabolic flux analysis reveals an unconventional pathway of fatty acid synthesis in cancer cells deficient for the mitochondrial citrate transport protein.
Article in Metabolic engineering, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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57 citing papers in PubMed, 85 citations in OpenAlex.
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- Modeling lipid homeostasis using stable isotope tracing and flux analysis.Cell metabolism · 2026Article
- The Interdependence of Carbon Substrates and Metabolic Pathways Enables the Metabolic Plasticity of Cancer Cells.Advances in experimental medicine and biology · 2026Review
- Metabolic Symbiosis Between Cancer Cells and Endothelial Cells: A Key Driver of Tumor Angiogenesis.Advances in experimental medicine and biology · 2026Review
- Exploring the significance of fatty acid metabolism reprogramming in the pathogenesis of cancer and anticancer therapy.Annals of medicine · 2025Review
- Inhibition of scheggia/SLC25A1 citrate transporter alleviates XPD deficits.Scientific reports · 2025Article
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- Inactivation of the SLC25A1 gene during embryogenesis induces a unique senescence program controlled by p53.Cell death and differentiation · 2025Article
- Instationary metabolic flux analysis reveals that NPC1 inhibition increases glycolysis and decreases mitochondrial metabolism in brain microvascular endothelial cells.Neurobiology of disease · 2025Article
- Hyperpolarized MRI theranostics in cancer.Frontiers in oncology · 2025Article
- The Role of Mitochondrial Solute Carriers SLC25 in Cancer Metabolic Reprogramming: Current Insights and Future Perspectives.International journal of molecular sciences · 2024Review
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- Citrate: a key signalling molecule and therapeutic target for bone remodeling disorder.Frontiers in endocrinology · 2024Review
- A comprehensive analysis of SLC25A1 expression and its oncogenic role in pan-cancer.Discover oncology · 2023Article
- Combined Inhibition ofInternational journal of molecular sciences · 2023Article
- Interpreting metabolic complexity via isotope-assisted metabolic flux analysis.Trends in biochemical sciences · 2023Review
- Isotope-Assisted Metabolic Flux Analysis: A Powerful Technique to Gain New Insights into the Human Metabolome in Health and Disease.Metabolites · 2022Review
- SLC16A7 Promotes Triglyceride Deposition by De Novo Lipogenesis in Chicken Muscle Tissue.Biology · 2022Article
- Metabolic reprogramming in the OPA1-deficient cells.Cellular and molecular life sciences : CMLS · 2022Article
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Authors and funding
8 authors at 3 institutions in 2 countries.
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Abstract
The mitochondrial citrate transport protein (CTP), encoded by SLC25A1, accommodates bidirectional trafficking of citrate between the mitochondria and cytosol, supporting lipid biosynthesis and redox homeostasis. Genetic CTP deficiency causes a fatal neurodevelopmental syndrome associated with the accumulation of L- and D-2-hydroxyglutaric acid, and elevated CTP expression is associated with poor prognosis in several types of cancer, emphasizing the importance of this transporter in multiple human pathologies. Here we describe the metabolic consequences of CTP deficiency in cancer cells. As expected from the phenotype of CTP-deficient humans, somatic CTP loss in cancer cells induces broad dysregulation of mitochondrial metabolism, resulting in accumulation of lactate and of the L- and D- enantiomers of 2-hydroxyglutarate (2HG) and depletion of TCA cycle intermediates. It also eliminates mitochondrial import of citrate from the cytosol. To quantify the impact of CTP deficiency on metabolic flux, cells were cultured with a set of
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