ArticleNature communications2022
MYC sensitises cells to apoptosis by driving energetic demand.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Review
- Toosendanin suppresses acute myeloid leukemia by targeting DDX5/c-Myc axis to inhibit protein synthesis.Journal of translational medicine · 2026Article
- NRIP1 disrupts ERα signal in Sjögren's disease via AQP5 suppression and MYC-driven salivary dysfunction.Experimental & molecular medicine · 2026Article
- Characterization and Clinical Diagnostic Potential of IHRDEGs in Renal Interstitial Fibrosis: An Integrative Data Analysis and Model Construction Study.Journal of inflammation research · 2026Article
- Epstein-Barr virus-associated tumors: commonalities in pathogenesis and the tumor immune microenvironment.Frontiers in immunology · 2026Review
- Article
- Antitumor Effects of Quercetin and Luteolin in A375 Cutaneous Melanoma Cell Line Are Mediated by Upregulation of P-ERK, c-Myc, and the Upstream GPER.Life (Basel, Switzerland) · 2025Article
- Arginine: at the crossroads of nitrogen metabolism.The EMBO journal · 2025Review
- Integrative multi-omics analysis reveals the interaction mechanisms between gut microbiota metabolites and ferroptosis in rheumatoid arthritis.Frontiers in immunology · 2025Article
- In vivo Therapeutic Inhibition of the Tp53-Induced Glycolysis and Apoptosis Regulator (TIGAR) by Intravenous Administration of an Anti-Oncological siRNA-Biopolymer, TI6752 (Tituxistatin), in a Preclinical Xenograft Model of Colorectal Cancer.Journal of experimental pharmacology · 2025Article
- Exploiting replication stress for synthetic lethality in MYC-driven cancers.American journal of cancer research · 2025Review
- The Interplay Between theInternational journal of molecular sciences · 2024Review
- Article
- [Latest Findings on the Role of α-Ketoglutarate in Metabolic Syndrome].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2024Review
- Ultrasound-responsive spherical nucleic acid against c-Myc/PD-L1 to enhance anti-tumoral macrophages in triple-negative breast cancer progression.Science China. Life sciences · 2024Article
- Pan-cancer evaluation of regulated cell death to predict overall survival and immune checkpoint inhibitor response.NPJ precision oncology · 2024Article
- Chronic lymphocytic leukemia patient-derived xenografts recapitulate clonal evolution to Richter transformation.Leukemia · 2024Article
- Metabolite itaconate in host immunoregulation and defense.Cellular & molecular biology letters · 2023Review
- The promoting effect and mechanism of MAD2L2 on stemness maintenance and malignant progression in glioma.Journal of translational medicine · 2023Article
- Article
Corrections and comments
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Authors and funding
33 authors.
Funding
Abstract
The MYC oncogene is a potent driver of growth and proliferation but also sensitises cells to apoptosis, which limits its oncogenic potential. MYC induces several biosynthetic programmes and primary cells overexpressing MYC are highly sensitive to glutamine withdrawal suggesting that MYC-induced sensitisation to apoptosis may be due to imbalance of metabolic/energetic supply and demand. Here we show that MYC elevates global transcription and translation, even in the absence of glutamine, revealing metabolic demand without corresponding supply. Glutamine withdrawal from MRC-5 fibroblasts depletes key tricarboxylic acid (TCA) cycle metabolites and, in combination with MYC activation, leads to AMP accumulation and nucleotide catabolism indicative of energetic stress. Further analyses reveal that glutamine supports viability through TCA cycle energetics rather than asparagine biosynthesis and that TCA cycle inhibition confers tumour suppression on MYC-driven lymphoma in vivo. In summary, glutamine supports the viability of MYC-overexpressing cells through an energetic rather than a biosynthetic mechanism.
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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.