ArticleMolecular systems biology2012
Glucose deprivation activates a metabolic and signaling amplification loop leading to cell death.
Article in Molecular systems biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
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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.
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Who cites it
104 citing papers in PubMed, 213 citations in OpenAlex.
- Hormetic fasting extends Caenorhabditis elegans lifespan via H3K27 acetylation of lipid catabolism and antioxidant genes.Cell reports · 2026Article
- Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.Nature communications · 2026Article
- Starvation of leukemic cells enhances DNA damage-induced apoptosis in vitro via ROS/p38 MAPK and prevents leukemia progression in fasting xenograft mice.The Journal of biological chemistry · 2026Article
- Mannose metabolic pathway senses glucose supply and regulates cell fate decisions.The Journal of biological chemistry · 2026Article
- Tumor metabolic adaptation induced by L-asparaginase reveals a vulnerability to PARP1/2 inhibitor in B-cell lymphomas.Nature communications · 2026Article
- Hormetic nutrient stress promotes longevity by orchestrating histone acetylation on key lipid catabolism and antioxidant defense genes.bioRxiv : the preprint server for biology · 2025Article
- Structural and systems characterization of phosphorylation on metabolic enzymes identifies sex-specific metabolic reprogramming in obesity.Molecular cell · 2025Article
- GPVI-dependent functional competence of buffy coat platelet concentrates (PCs) versus PRP-derived PCs: insights into the effects of biomechanical forces during platelet preparation.Annals of hematology · 2025Article
- D-ribose-5-phosphate inactivates YAP and functions as a metabolic checkpoint.Journal of hematology & oncology · 2025Article
- Mechanisms and therapeutic potential of disulphidptosis in cancer.Cell proliferation · 2025Review
- Variations in the fetal bovine serum and glucose concentration in the culture medium impact the viability of glioblastoma cells as evidenced through the modulation of cell cycle and reactive oxygen species: AnJournal of biological methods · 2025Article
- Insights from a multiscale framework on metabolic rate variation driving glioblastoma multiforme growth and invasion.Communications engineering · 2024Article
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- PANAMA-enabled high-sensitivity dual nanoflow LC-MS metabolomics and proteomics analysis.Cell reports methods · 2024Article
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- Oxidative Stress in Breast Cancer: A Biochemical Map of Reactive Oxygen Species Production.Current issues in molecular biology · 2024Review
- RIOK3 sustains colorectal cancer cell survival under glucose deprivation via an HSP90α-dependent pathway.Oncogenesis · 2024Article
- Corneal Vascularization Associated With a Novel PDGFRB Variant.Investigative ophthalmology & visual science · 2023Article
- Metabolic Phenotype Intricacies on Altered Glucose Metabolism of Breast Cancer Cells upon Glut-1 Inhibition and Mimic Hypoxia In Vitro.Applied biochemistry and biotechnology · 2023Article
44 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
The altered metabolism of cancer can render cells dependent on the availability of metabolic substrates for viability. Investigating the signaling mechanisms underlying cell death in cells dependent upon glucose for survival, we demonstrate that glucose withdrawal rapidly induces supra-physiological levels of phospho-tyrosine signaling, even in cells expressing constitutively active tyrosine kinases. Using unbiased mass spectrometry-based phospho-proteomics, we show that glucose withdrawal initiates a unique signature of phospho-tyrosine activation that is associated with focal adhesions. Building upon this observation, we demonstrate that glucose withdrawal activates a positive feedback loop involving generation of reactive oxygen species (ROS) by NADPH oxidase and mitochondria, inhibition of protein tyrosine phosphatases by oxidation, and increased tyrosine kinase signaling. In cells dependent on glucose for survival, glucose withdrawal-induced ROS generation and tyrosine kinase signaling synergize to amplify ROS levels, ultimately resulting in ROS-mediated cell death. Taken together, these findings illustrate the systems-level cross-talk between metabolism and signaling in the maintenance of cancer cell homeostasis.
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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.