Evidence map›Paper›PMID 29594839›Full record

ReviewJournal of bioenergetics and biomembranes2018

O-GlcNAc in cancer: An Oncometabolism-fueled vicious cycle.

John A Hanover, Weiping Chen, Michelle R Bond

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of bioenergetics and biomembranes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed
7.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

82 citing papers in PubMed, 147 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Glucosamine as a regulator of O-GlcNAc signaling: linking metabolism to disease pathogenesis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  14. Article
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  18. Article
  19. Targeted Protein O-GlcNAcylation Using Bifunctional Small Molecules.Journal of the American Chemical Society · 2024
    Article
  20. Review

22 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

John A HanoverLaboratory of Cell Biochemistry and Molecular Biology, NIDDK, NIH, Bldg 8 Rm B1 27, 9000 Rockville Pike, Bethesda, MD, 20892-0851, USA. jah@helix.nih.gov.ORCID 0000-0002-3154-9878
Weiping ChenNIDDK Genomics Core, Bethesda, MD, USA.
Michelle R BondLaboratory of Cell Biochemistry and Molecular Biology, NIDDK, NIH, Bldg 8 Rm B1 27, 9000 Rockville Pike, Bethesda, MD, 20892-0851, USA.
ID Genomics (United States) · USNational Institutes of Health · US

Funding

Targeted disruption the enzymes of O-GlcNAc cycling: Animal models of DiseaseZIADK060101 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$25.7M
Enzymes of O-GlcNAc cycling linked to type-2 diabetes and neurodegenerationZIADK060103 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$20.8M
Calmodulin-driven Nuclear Trafficking linked to diabetes and insulin signalingZIADK060102 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2025
$8.5M
NIDDK NIH HHS intramural funds
6 · The paper itself

Abstract

Cancer cells exhibit unregulated growth, altered metabolism, enhanced metastatic potential and altered cell surface glycans. Fueled by oncometabolism and elevated uptake of glucose and glutamine, the hexosamine biosynthetic pathway (HBP) sustains glycosylation in the endomembrane system. In addition, the elevated pools of UDP-GlcNAc drives the O-GlcNAc modification of key targets in the cytoplasm, nucleus and mitochondrion. These targets include transcription factors, kinases, key cytoplasmic enzymes of intermediary metabolism, and electron transport chain complexes. O-GlcNAcylation can thereby alter epigenetics, transcription, signaling, proteostasis, and bioenergetics, key 'hallmarks of cancer'. In this review, we summarize accumulating evidence that many cancer hallmarks are linked to dysregulation of O-GlcNAc cycling on cancer-relevant targets. We argue that onconutrient and oncometabolite-fueled elevation increases HBP flux and triggers O-GlcNAcylation of key regulatory enzymes in glycolysis, Kreb's cycle, pentose-phosphate pathway, and the HBP itself. The resulting rerouting of glucose metabolites leads to elevated O-GlcNAcylation of oncogenes and tumor suppressors further escalating elevation in HBP flux creating a 'vicious cycle'. Downstream, elevated O-GlcNAcylation alters DNA repair and cellular stress pathways which influence oncogenesis. The elevated steady-state levels of O-GlcNAcylated targets found in many cancers may also provide these cells with a selective advantage for sustained growth, enhanced metastatic potential, and immune evasion in the tumor microenvironment.

Indexed as

AcetylglucosamineAnimalsBiosynthetic PathwaysGlycosylationHumansNeoplasmsAcetylglucosamineCancerDNA damageEpigeneticsGlycolysisHexosamine biosythetic pathwayO-GlcNAcOncogenesOncometabolismOxidative phosphorylationTumor suppressors

Identifiers

PMID29594839
OpenAlexW2795743867

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.