ArticleOncotarget2015
Elevated O-GlcNAcylation promotes colonic inflammation and tumorigenesis by modulating NF-κB signaling.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 86 citations in OpenAlex.
- 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.] · 2026Review
- OGT-Mediated O-GlcNAcylation Stabilizes c-Myc Activity and Promotes Chemoresistance in Triple-Negative Breast Cancer.The breast journal · 2026Article
- Intestinal Mucin Glycosylation: Structural Regulation, Homeostasis Maintenance and Disease Association.Biomolecules · 2025Review
- O‑GlcNAcylation as an emerging molecular target for cholangiocarcinoma therapy (Review).Oncology reports · 2025Review
- Taurine alleviates colitis by regulating oxidative stress, inflammatory responses, ER stress, and apoptotic pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Glycosylation in kidney diseases.Precision clinical medicine · 2025Review
- O-GlcNAcylation: roles and potential therapeutic target for bone pathophysiology.Cell communication and signaling : CCS · 2024Review
- Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024Review
- Identification of O-glycosylation related genes and subtypes in ulcerative colitis based on machine learning.PloS one · 2024Article
- The correlation between cellular O-GlcNAcylation and sensitivity to O-GlcNAc inhibitor in colorectal cancer cells.PloS one · 2024Article
- 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
- O-GlcNAcylation and Its Role in Cancer-Associated Inflammation.Frontiers in immunology · 2022Review
- ProteinFrontiers in immunology · 2022Review
- Inhibition of O-GlcNAc transferase sensitizes prostate cancer cells to docetaxel.Frontiers in oncology · 2022Article
- Inhibition of O-GlcNAcylation Decreases the Cytotoxic Function of Natural Killer Cells.Frontiers in immunology · 2022Article
- Article
- An integrative network analysis framework for identifying molecular functions in complex disorders examining major depressive disorder as a test case.Scientific reports · 2021Article
- Targeted deletion of Atg5 in intestinal epithelial cells promotes dextran sodium sulfate-induced colitis.Journal of clinical biochemistry and nutrition · 2021Article
- Regulation of Nuclear Factor-kappaB Function byFrontiers in cell and developmental biology · 2021Review
- The Dysregulation of OGT/OGA Cycle Mediates Tau and APP Neuropathology in Down Syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
O-GlcNAcylation is a reversible post-translational modification. O-GlcNAc addition and removal is catalyzed by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA), respectively. More recent evidence indicates that regulation of O-GlcNAcylation is important for inflammatory diseases and tumorigenesis. In this study, we revealed that O-GlcNAcylation was increased in the colonic tissues of dextran sodium sulfate (DSS)-induced colitis and azoxymethane (AOM)/DSS-induced colitis-associated cancer (CAC) animal models. Moreover, the O-GlcNAcylation level was elevated in human CAC tissues compared with matched normal counterparts. To investigate the functional role of O-GlcNAcylation in colitis, we used OGA heterozygote mice, which have an increased level of O-GlcNAcylation. OGA(+/-) mice have higher susceptibility to DSS-induced colitis than OGA(+/+) mice. OGA(+/-) mice exhibited a higher incidence of colon tumors than OGA(+/+) mice. In molecular studies, elevated O-GlcNAc levels were shown to enhance the activation of NF-κB signaling through increasing the binding of RelA/p65 to its target promoters. We also found that Thr-322 and Thr352 in the p65-O-GlcNAcylation sites are critical for p65 promoter binding. These results suggest that the elevated O-GlcNAcylation level in colonic tissues contributes to the development of colitis and CAC by disrupting regulation of NF-κB-dependent transcriptional activity.
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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.