ReviewCancer letters2015
O-GlcNAc signaling in cancer metabolism and epigenetics.
Review in Cancer letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers.
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.
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.
Who cites it
86 citing papers in PubMed, 133 citations in OpenAlex.
- Emerging roles of O-GlcNAcylation in tumorigenesis, immunosuppression and drug resistance (Review).Oncology letters · 2026Review
- Identification of TMEM115 as a tumor suppressor gene and clinical prognostic factor that influences TERT expression in pancreatic cancer.Scientific reports · 2026Article
- Circular RNAs: Key Regulators of Tumor Metabolic Reprogramming and Clinical Translation.Oncology research · 2026Review
- Epigenetic co-regulator HCF-1 promotes lung cancer via O-GlcNAcylation-dependent pathways.Molecular therapy. Oncology · 2025Article
- GNPNAT1 acts as a prognostic biomarker associated with immune infiltration in lung adenocarcinoma and promotes the proliferation and invasion of cancer cells.Discover oncology · 2025Article
- Crosstalk between O-GlcNAcylation and phosphorylation in metabolism: regulation and mechanism.Cell death and differentiation · 2025Review
- Exploring biomarkers and molecular mechanisms of Type 2 diabetes mellitus promotes colorectal cancer progression based on transcriptomics.Scientific reports · 2025Article
- FTO O-GlcNAcylation promotes TRIM21-mediated FTO ubiquitination degradation to sustain the negative feedback control of macrophage inflammation.Frontiers in immunology · 2025Article
- FUT2 promotes colorectal cancer metastasis by reprogramming fatty acid metabolism via YAP/TAZ signaling and SREBP-1.Communications biology · 2024Article
- A protein O-GlcNAc glycosyltransferase regulates the antioxidative response in Yersinia pestis.Nature communications · 2024Article
- O-GlcNAcase regulates pluripotency states of human embryonic stem cells.Stem cell reports · 2024Article
- Regulation of Hypoxia Dependent Reprogramming of Cancer Metabolism: Role of HIF-1 and Its Potential Therapeutic Implications in Leukemia.Asian Pacific journal of cancer prevention : APJCP · 2024Review
- Hexosamine biosynthesis and related pathways, protein N-glycosylation and O-GlcNAcylation: their interconnection and role in plants.Frontiers in plant science · 2024Review
- Review
- O-GlcNAcylation Is Required for the Survival of Cerebellar Purkinje Cells by Inhibiting ROS Generation.Antioxidants (Basel, Switzerland) · 2023Article
- Polo-like kinase 1 (PLK1) O-GlcNAcylation is essential for dividing mammalian cells and inhibits uterine carcinoma.The Journal of biological chemistry · 2023Article
- IDH2, a novel target of OGT, facilitates glucose uptake and cellular bioenergy production via NF-κB signaling to promote colorectal cancer progression.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Epimutations and Their Effect on Chromatin Organization: Exciting Avenues for Cancer Treatment.Cancers · 2022Review
- Metabolic reprogramming and epigenetic modifications on the path to cancer.Protein & cell · 2022Review
- Review
26 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
4 authors at 1 institution in 1 country.
Funding
Abstract
The covalent attachment of β-D-N-acetylglucosamine monosaccharides (O-GlcNAc) to serine/threonine residues of nuclear and cytoplasmic proteins is a major regulatory mechanism in cell physiology. Aberrant O-GlcNAc modification of signaling proteins, metabolic enzymes, and transcriptional and epigenetic regulators has been implicated in cancer. Relentless growth of cancer cells requires metabolic reprogramming that is intertwined with changes in the epigenetic landscape. This review highlights the emerging role of protein O-GlcNAcylation at the interface of cancer metabolism and epigenetics.
Indexed as
Identifiers
What OpenQuestion holds
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.