ArticleOncogene2009
c-Myc activates multiple metabolic networks to generate substrates for cell-cycle entry.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
102 citing papers in PubMed, 166 citations in OpenAlex.
- Local production of lactate, ribose phosphate, and amino acids within human triple-negative breast cancer.Med (New York, N.Y.) · 2021Trial
- Article
- Crosstalk BetweenCancers · 2026Review
- The GFPT2/O-GlcNAcylation/c-Myc axis promotes bladder cancer progression.Journal of translational medicine · 2026Article
- Enzyme Assemblies in Nucleotide Metabolism: Structure, Regulation, and Disease Implications.Advances in experimental medicine and biology · 2026Review
- Concordant RNA-protein evidence and human tissue metabolomics prioritize UPP1-associated nucleotide remodeling in prostate cancer.PloS one · 2026Article
- O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review).Oncology reports · 2025Review
- Targeting MYC: Multidimensional regulation and therapeutic strategies in oncology.Genes & diseases · 2025Review
- Elevated choline drives KLF5-dominated transcriptional reprogramming to facilitate liver cancer progression.Oncogene · 2024Article
- The Use of Patient-Derived Organoids in the Study of Molecular Metabolic Adaptation in Breast Cancer.International journal of molecular sciences · 2024Review
- Nucleophosmin 1 cooperates with BRD4 to facilitate c-Myc transcription to promote prostate cancer progression.Cell death discovery · 2023Article
- Review
- The "Superoncogene" Myc at the Crossroad between Metabolism and Gene Expression in Glioblastoma Multiforme.International journal of molecular sciences · 2023Review
- PI3K/ c-Myc/AFF4 axis promotes pancreatic tumorigenesis through fueling nucleotide metabolism.International journal of biological sciences · 2023Article
- Deregulated transcription factors in cancer cell metabolisms and reprogramming.Seminars in cancer biology · 2022Review
- Costimulatory CD226 Signaling Regulates Proliferation of Memory-like NK Cells in Healthy Individuals with LatentInternational journal of molecular sciences · 2022Article
- MYC sensitises cells to apoptosis by driving energetic demand.Nature communications · 2022Article
- Article
- Metabolic requirements of NK cells during the acute response against retroviral infection.Nature communications · 2021Article
- Review
42 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
5 authors at 4 institutions in 1 country.
Funding
Abstract
Cell proliferation requires the coordinated activity of cytosolic and mitochondrial metabolic pathways to provide ATP and building blocks for DNA, RNA and protein synthesis. Many metabolic pathway genes are targets of the c-myc oncogene and cell-cycle regulator. However, the contribution of c-Myc to the activation of cytosolic and mitochondrial metabolic networks during cell-cycle entry is unknown. Here, we report the metabolic fates of [U-(13)C] glucose in serum-stimulated myc(-/-) and myc(+/+) fibroblasts by (13)C isotopomer NMR analysis. We demonstrate that endogenous c-myc increased (13)C labeling of ribose sugars, purines and amino acids, indicating partitioning of glucose carbons into C1/folate and pentose phosphate pathways, and increased tricarboxylic acid cycle turnover at the expense of anaplerotic flux. Myc expression also increased global O-linked N-acetylglucosamine protein modification, and inhibition of hexosamine biosynthesis selectively reduced growth of Myc-expressing cells, suggesting its importance in Myc-induced proliferation. These data reveal a central organizing function for the Myc oncogene in the metabolism of cycling cells. The pervasive deregulation of this oncogene in human cancers may be explained by its function in directing metabolic networks required for cell proliferation.
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What OpenQuestion holds
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.