ArticleNature communications2015
O-GlcNAcylation of G6PD promotes the pentose phosphate pathway and tumor growth.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 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.
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Who cites it
154 citing papers in PubMed, 255 citations in OpenAlex.
- A conserved eIF1ACell reports. Medicine · 2026Trial
- A Function-Centric Framework for Mitochondrial Quality Control.Biomolecules · 2026Review
- O-GlcNAcylation: the metabolic-immune translator in tumor evolution and treatment.Molecular medicine (Cambridge, Mass.) · 2026Review
- SUMOylation-stabilized G6PD orchestrates metabolic rewiring for oxidative stress survival and chemoresistance in HCC via a PKCδ-phosphorylation trigger.Cell death and differentiation · 2026Article
- Glucose-6-Phosphate Dehydrogenase Modifies the Impact of Glucose on Arterial Aging in A Sex-Specific Manner.Journal of the American Heart Association · 2026Article
- CircNOLC1/KRT16 promotes colorectal cancer invasion and migration via c-met nuclear translocation and reprogramming of the oxidative pentose phosphate pathway.The Journal of biological chemistry · 2026Article
- TargetingbioRxiv : the preprint server for biology · 2025Article
- Cell cycle regulation in cancer cells by O-GlcNAcylation.Glycoconjugate journal · 2025Review
- Epigenetic Regulation of G6PD Drives Metabolic Reprogramming in Intrahepatic Cholangiocarcinoma.Cancer science · 2025Article
- Elevating cytosolic NADPH metabolism in endothelial cells ameliorates vascular aging.Nature communications · 2025Article
- Ferroptosis in Diabetic Cardiomyopathy and Atherosclerosis: Mechanisms and Clinical Prospects.International journal of molecular sciences · 2025Review
- Deacetylation of TALDO1 by HDAC6 promotes glycolysis and nasopharyngeal carcinoma progression through a moonlighting function.Cell death & disease · 2025Article
- O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review).Oncology reports · 2025Review
- The lactylation of glucose-6-phosphate dehydrogenase promotes malignant phenotypes in cancer cell lines.Molecular biology reports · 2025Article
- Article
- A ROS-mediated oxidation-O-GlcNAcylation cascade governs ferroptosis.Nature cell biology · 2025Article
- HPD is an RNA-Binding Protein Sustaining Ovarian Cancer Cell Glycolysis, Tumor Growth, and Drug Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Unraveling the nexus: Genomic instability and metabolism in cancer.Cell reports · 2025Review
- Hypoxia-Induced O-GlcNAcylation of GATA3 Leads to Excessive Testosterone Production in Preeclamptic Placentas.MedComm · 2025Article
- Recent Progress of Small-molecule Inhibitors of O-GlcNAcase for Alzheimer's Disease.Mini reviews in medicinal chemistry · 2025Review
94 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
13 authors at 4 institutions in 2 countries.
Funding
Abstract
The pentose phosphate pathway (PPP) plays a critical role in macromolecule biosynthesis and maintaining cellular redox homoeostasis in rapidly proliferating cells. Upregulation of the PPP has been shown in several types of cancer. However, how the PPP is regulated to confer a selective growth advantage on cancer cells is not well understood. Here we show that glucose-6-phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the PPP, is dynamically modified with an O-linked β-N-acetylglucosamine sugar in response to hypoxia. Glycosylation activates G6PD activity and increases glucose flux through the PPP, thereby providing precursors for nucleotide and lipid biosynthesis, and reducing equivalents for antioxidant defense. Blocking glycosylation of G6PD reduces cancer cell proliferation in vitro and impairs tumor growth in vivo. Importantly, G6PD glycosylation is increased in human lung cancers. Our findings reveal a mechanistic understanding of how O-glycosylation directly regulates the PPP to confer a selective growth advantage to tumours.
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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.