ArticleInternational journal of molecular sciences2023
Glucose Deprivation Induces Cancer Cell Death through Failure of ROS Regulation.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Collagen I promotes cancer cell survival via amino acid import and mTORC1/S6 activation.PLoS biology · 2026Article
- Inhibiting Fatty Acid Oxidation Reverses Autophagy-Mediated Acquired Chemotherapy Resistance in Pancreatic Ductal Adenocarcinoma.Cancer research · 2026Article
- Glucose transport dependency defines a therapeutic vulnerability in JAK2V617F-driven myeloproliferative neoplasms.Cell communication and signaling : CCS · 2026Article
- Infection-induced glucose starvation triggers NINJ1-dependent macrophage lysis and Candida escape.Nature communications · 2026Article
- ARHGEF7 S-glutathionylation promotes cancer cell migration through Rac1 activation.bioRxiv : the preprint server for biology · 2026Article
- Nanomedicine-enabled disruption of glucose metabolism and synergistic antitumor therapy.Journal of nanobiotechnology · 2026Review
- 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
- Redox regulation of cell migration via Nischarin S-glutathionylation.Free radical biology & medicine · 2026Article
- Glucose oxidase-powered nanocatalytic medicine: Rewiring tumor metabolism for multimodal cancer therapy.Materials today. Bio · 2026Review
- A nutrient-responsive cancer-on-chip model for assessing chemotherapy responses under glucose restriction.Frontiers in bioengineering and biotechnology · 2026Article
- Energy stress-induced PKCζ S-glutathionylation is essential for LKB1 cytoplasmic translocation and AMPK activation.Life metabolism · 2025Article
- Combined Effects of Atorvastatin and Glucose Deprivation on Metabolic Stress and Lipid-Raft Disruption in Glioblastoma and Breast Cancer Cells.Pharmaceutics · 2025Article
- YULINK deficiency promotes cell death under glucose restriction in HCC cells in association with GLUT1-mediated glycolysis.Molecular medicine (Cambridge, Mass.) · 2025Article
- Redox Regulation of Cell Migration via Nischarin S-glutathionylation.bioRxiv : the preprint server for biology · 2025Article
- Programmed Cell Death in Cancer.MedComm · 2025Review
- A Smart Nanomedicine Unleashes a Dual Assault of Glucose Starvation and Cuproptosis to Supercharge αPD-L1 Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Loss ofTheranostics · 2025Article
- Ketogenic Interventions in Autosomal Dominant Polycystic Kidney Disease: A Comprehensive Review of Current Evidence.Nutrients · 2024Review
- Glycooligomer-Functionalized Catalytic Nanocompartments Co-Loaded with Enzymes Support Parallel Reactions and Promote Cell Internalization.Biomacromolecules · 2024Article
- APC/C-regulated CPT1C promotes tumor progression by upregulating the energy supply and accelerating the G1/S transition.Cell communication and signaling : CCS · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
In previous work, we showed that cancer cells do not depend on glycolysis for ATP production, but they do on fatty acid oxidation. However, we found some cancer cells induced cell death after glucose deprivation along with a decrease of ATP production. We investigated the different response of glucose deprivation with two types of cancer cells including glucose insensitive cancer cells (GIC) which do not change ATP levels, and glucose sensitive cancer cells (GSC) which decrease ATP production in 24 h. Glucose deprivation-induced cell death in GSC by more than twofold after 12 h and by up to tenfold after 24 h accompanied by decreased ATP production to compare to the control (cultured in glucose). Glucose deprivation decreased the levels of metabolic intermediates of the pentose phosphate pathway (PPP) and the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) in both GSC and GIC. However, glucose deprivation increased reactive oxygen species (ROS) only in GSC, suggesting that GIC have a higher tolerance for decreased NADPH than GSC. The twofold higher ratio of reduced/oxidized glutathione (GSH/GSSG) in GIS than in GSC correlates closely with the twofold lower ROS levels under glucose starvation conditions. Treatment with N-acetylcysteine (NAC) as a precursor to the biologic antioxidant glutathione restored ATP production by 70% and reversed cell death caused by glucose deprivation in GSC. The present findings suggest that glucose deprivation-induced cancer cell death is not caused by decreased ATP levels, but rather triggered by a failure of ROS regulation by the antioxidant system. Conclusion is clear that glucose deprivation-induced cell death is independent from ATP depletion-induced cell death.
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