ArticleNature communications2024
mTORC1 regulates cell survival under glucose starvation through 4EBP1/2-mediated translational reprogramming of fatty acid metabolism.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- N7-Methylguanosine Modification in Colorectal Cancer: Molecular Insights and Clinical Implications.International journal of molecular sciences · 2026Review
- Glucose restriction reprograms lipid metabolism and enhances immunotherapy through ZNRF3-Wnt-SCD signaling axis.Journal for immunotherapy of cancer · 2026Article
- Multi-omic analysis of the liver-breast axis reveals key hepatic mediators of breast cancer progression.Science China. Life sciences · 2026Review
- Mitochondrial ETF insufficiency drives neoplastic growth by selectively optimizing cancer bioenergetics.eLife · 2026Article
- TRIM24 Regulates Adaptation to Glucose Deprivation in Association with Aspartate Accumulation and Impaired AMPK Signaling.Current issues in molecular biology · 2026Article
- Autophagosome marker, LC3, is released extracellularly via several distinct pathways.FEBS open bio · 2026Article
- Early Postreperfusion Proteomics Reveal Divergent Inflammatory Responses in Kidney Transplantation With Implications on Outcomes.Transplantation · 2026Article
- Targeting tumor transition windows.Exploration of targeted anti-tumor therapy · 2026Review
- Intracellular IL-24 ameliorates lipid metabolic disorders in metabolic dysfunction-associated steatohepatitis by restoring the autophagy-lysosome pathway.Cellular and molecular life sciences : CMLS · 2025Article
- KIF11 variants in familial exudative vitreoretinopathy leading to mTORC1 overactivation and impaired cell cycle progression.Human genomics · 2025Article
- Dual-Target Insight into Drug Discovery from Natural Products as Modulators of GLP-1 and the TXNIP-Thioredoxin Antioxidant System in Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2025Review
- ORMDL2 Promotes the Growth of Glioma through mTORC1-Mediated Fatty Acid Metabolism.Applied biochemistry and biotechnology · 2025Article
- Programmed Cell Death in Cancer.MedComm · 2025Review
- Peroxisomal lipid metabolism inhibits Pimozide-induced cancer cell death by regulating ATP homeostasis.Oncogenesis · 2025Article
- Short-Term Severe Energy Restriction Promotes Molecular Health and Reverses Aging Signatures in Adults With Prediabetes in the PREVIEW Study.Aging cell · 2025Article
- Review
- Neural stimulation suppresses mTORC1-mediated protein synthesis in skeletal muscle.Science advances · 2025Article
- eIF4F-mediated dysregulation of mRNA translation in cancer.RNA (New York, N.Y.) · 2025Review
- Article
- lncRNAs: the unexpected link between protein synthesis and cancer adaptation.Molecular cancer · 2025Review
Corrections and comments
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Authors and funding
31 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Energetic stress compels cells to evolve adaptive mechanisms to adjust their metabolism. Inhibition of mTOR kinase complex 1 (mTORC1) is essential for cell survival during glucose starvation. How mTORC1 controls cell viability during glucose starvation is not well understood. Here we show that the mTORC1 effectors eukaryotic initiation factor 4E binding proteins 1/2 (4EBP1/2) confer protection to mammalian cells and budding yeast under glucose starvation. Mechanistically, 4EBP1/2 promote NADPH homeostasis by preventing NADPH-consuming fatty acid synthesis via translational repression of Acetyl-CoA Carboxylase 1 (ACC1), thereby mitigating oxidative stress. This has important relevance for cancer, as oncogene-transformed cells and glioma cells exploit the 4EBP1/2 regulation of ACC1 expression and redox balance to combat energetic stress, thereby supporting transformation and tumorigenicity in vitro and in vivo. Clinically, high EIF4EBP1 expression is associated with poor outcomes in several cancer types. Our data reveal that the mTORC1-4EBP1/2 axis provokes a metabolic switch essential for survival during glucose starvation which is exploited by transformed and tumor cells.
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