ArticleThe Journal of biological chemistry2009
O-GlcNAc protein modification in cancer cells increases in response to glucose deprivation through glycogen degradation.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 85 citations in OpenAlex.
- Cross-talk between glycosylation pathways: Mechanistic insights and implications for human diseases.Molecular metabolism · 2026Review
- Starvation-induced HSC70 O-GlcNAcylation activates chaperone-mediated autophagy.The Journal of biological chemistry · 2026Article
- Understanding O-GlcNAc transferase (OGT): Every amino acid matters.The Journal of biological chemistry · 2025Review
- ULK1-dependent phosphorylation of OGT instructs the tumorigenicity of O-GlcNAcylation.Science China. Life sciences · 2025Article
- Downregulation of O-GlcNAcylation enhances etoposide-induced p53-mediated apoptosis in HepG2 human liver cancer cells.FEBS open bio · 2025Article
- Carbohydrate-Binding Properties and Antimicrobial and Anticancer Potential of a New Lectin from the Phloem Sap ofMolecules (Basel, Switzerland) · 2024Article
- Current knowledge and potential intervention of hexosamine biosynthesis pathway in lung cancer.World journal of surgical oncology · 2023Review
- Enzymatic assay for UDP-GlcNAc and its application in the parallel assessment of substrate availability and protein O-GlcNAcylation.Cell reports methods · 2023Article
- Nutrient sensors and their crosstalk.Experimental & molecular medicine · 2023Review
- O-GlcNAc modification of leucyl-tRNA synthetase 1 integrates leucine and glucose availability to regulate mTORC1 and the metabolic fate of leucine.Nature communications · 2022Article
- High-Fat Diet Leads to Reduced Protein O-GlcNAcylation and Mitochondrial Defects Promoting the Development of Alzheimer's Disease Signatures.International journal of molecular sciences · 2021Article
- Role ofPhysiological reviews · 2021Review
- Regulation of O-GlcNAcylation on endothelial nitric oxide synthase by glucose deprivation and identification of its O-GlcNAcylation sites.Scientific reports · 2020Article
- Article
- McArdle Disease: New Insights into Its Underlying Molecular Mechanisms.International journal of molecular sciences · 2019Review
- Cell Metabolism Control Through O-GlcNAcylation of STAT5: A Full or Empty Fuel Tank Makes a Big Difference for Cancer Cell Growth and Survival.International journal of molecular sciences · 2019Review
- O-GlcNAc-induced nuclear translocation of hnRNP-K is associated with progression and metastasis of cholangiocarcinoma.Molecular oncology · 2019Article
- dbPTM in 2019: exploring disease association and cross-talk of post-translational modifications.Nucleic acids research · 2019Article
- The Many Ways by WhichMolecules (Basel, Switzerland) · 2018Review
- "Nutrient-sensing" and self-renewal: O-GlcNAc in a new role.Journal of bioenergetics and biomembranes · 2018Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When cellular glucose concentrations fall below normal levels, in general the extent of protein O-GlcNAc modification (O-GlcNAcylation) decreases. However, recent reports demonstrated increased O-GlcNAcylation by glucose deprivation in HepG2 and Neuro-2a cells. Here, we report increased O-GlcNAcylation in non-small cell lung carcinoma A549 cells and various other cells in response to glucose deprivation. Although the level of O-GlcNAc transferase was unchanged, the enzyme contained less O-GlcNAc, and its activity was increased. Moreover, O-GlcNAcase activity was reduced. The studied cells contain glycogen, and we show that its degradation in response to glucose deprivation provides a source for UDP-GlcNAc required for increased O-GlcNAcylation under this condition. This required active glycogen phosphorylase and resulted in increased glutamine:fructose-6-phosphate amidotransferase, the first and rate-limiting enzyme in the hexosamine biosynthetic pathway. Interestingly, glucose deprivation reduced the amount of phosphofructokinase 1, a regulatory glycolytic enzyme, and blocked ATP synthesis. These findings suggest that glycogen is the source for increased O-GlcNAcylation but not for generating ATP in response to glucose deprivation and that this may be useful for cancer cells to survive.
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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.