ArticleMolecular systems biology2011
Oncogenic K-Ras decouples glucose and glutamine metabolism to support cancer cell growth.
Article in Molecular systems biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 314 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
314 citing papers in PubMed, 481 citations in OpenAlex.
- Targeting GLUTs in Cancer: Mechanisms, Combination Strategies, and Translational Challenges.Current medical science · 2026Review
- The RAB32-USP13 axis facilitates TOM40 mitochondrial localization to promote non-small cell lung cancer progression.Cell death and differentiation · 2026Article
- Decoy oligonucleotide technology in cancer therapy: molecular mechanisms, challenges, and translational potential.Medical oncology (Northwood, London, England) · 2026Review
- Boron-Doped Carbon Dots for Organelle Labeling and Mitochondrial Bioimaging.Methods and protocols · 2026Article
- Simvastatin reprograms lipid metabolism in B16.F10 melanoma cells to favor an early resistant phenotype.Scientific reports · 2026Article
- Article
- Regulation of Autophagy and Metabolism in Hepatocellular Carcinoma: Involvement of Wnt-β-Catenin Pathway.Journal of cellular and molecular medicine · 2026Article
- Lactate, a Spearhead of Cancer Aggressiveness: Metabolic Reprogramming, Immune Suppression, and Metastatic Progression.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2026Review
- FOXO1 links KRAS G12D and G12V alleles to glutamine and nitrogen metabolism in colorectal cancer.EMBO reports · 2026Article
- The role of gene duplication and paralog specialisation in the evolution of the mammalian PRPS complex.Nature communications · 2025Article
- Review
- Ras-dependent activation of BMAL2 regulates hypoxic metabolism in pancreatic cancer.bioRxiv : the preprint server for biology · 2025Article
- Overexpression of LSR suppresses glioma proliferation and invasion via regulating FOXO3a.Journal of neuro-oncology · 2025Article
- Fucoxanthin suppresses pancreatic cancer progression by inducing bioenergetics metabolism crisis and promoting SLC31A1‑mediated sensitivity to DDP.International journal of oncology · 2025Article
- Review
- A hormetic response model for glutamine stress in cancer.Trends in cancer · 2025Review
- Exploration of a prognostic signature for mitochondria-related genes and the therapeutic prospects of vorinostat in clear cell renal cell carcinoma.Translational andrology and urology · 2025Article
- Recent Anti-KRASCancers · 2025Review
- Exercise, cancer, and the cardiovascular system: clinical effects and mechanistic insights.Basic research in cardiology · 2025Review
- Metabolic Signaling in the Tumor Microenvironment.Cancers · 2025Review
254 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
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Oncogenes such as K-ras mediate cellular and metabolic transformation during tumorigenesis. To analyze K-Ras-dependent metabolic alterations, we employed ¹³C metabolic flux analysis (MFA), non-targeted tracer fate detection (NTFD) of ¹⁵N-labeled glutamine, and transcriptomic profiling in mouse fibroblast and human carcinoma cell lines. Stable isotope-labeled glucose and glutamine tracers and computational determination of intracellular fluxes indicated that cells expressing oncogenic K-Ras exhibited enhanced glycolytic activity, decreased oxidative flux through the tricarboxylic acid (TCA) cycle, and increased utilization of glutamine for anabolic synthesis. Surprisingly, a non-canonical labeling of TCA cycle-associated metabolites was detected in both transformed cell lines. Transcriptional profiling detected elevated expression of several genes associated with glycolysis, glutamine metabolism, and nucleotide biosynthesis upon transformation with oncogenic K-Ras. Chemical perturbation of enzymes along these pathways further supports the decoupling of glycolysis and TCA metabolism, with glutamine supplying increased carbon to drive the TCA cycle. These results provide evidence for a role of oncogenic K-Ras in the metabolic reprogramming of cancer cells.
Indexed as
Identifiers
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.