ArticleNature communications2017
The essential role of YAP O-GlcNAcylation in high-glucose-stimulated liver tumorigenesis.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers.
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Who cites it
150 citing papers in PubMed, 233 citations in OpenAlex.
- Targeting YAP: mechanistic breakthroughs and therapeutic prospects in reversing organ fibrosis.Molecular and cellular biochemistry · 2026Review
- Enhanced nuclear export caused by O-GlcNAcylation of nucleoporins is a potential therapeutic target in mesothelioma.British journal of cancer · 2026Article
- Subclonal β-catenin/YAP signaling heterogeneity accelerates ovarian cancer metastasis through a senescence-associated secretory phenotype.Cell death & disease · 2026Article
- Site-Specific and Quantitative O-GlcNAc Proteomics for Hepatocellular Carcinoma.Journal of proteome research · 2026Article
- YAP1 in control: how RNA networks and protein modifications shape its function and therapeutic targetability.Molecular cancer · 2026Review
- Nutrient Availability Dictates Cancer Metabolism-Based Therapeutic Responses to Nononcology Drugs.Cancer research · 2026Article
- Protein O-GlcNAcylation in Health and Diseases.MedComm · 2025Review
- The Hippo signaling pathway as a therapeutic target in Alzheimer's disease.Molecular neurodegeneration · 2025Review
- YAP/TAZ: An epitome of tumorigenesis.Cancer letters · 2025Review
- Posttranslational modifications of YAP/TAZ: molecular mechanisms and therapeutic opportunities.Cellular & molecular biology letters · 2025Review
- O-GlcNAcylation with ubiquitination stabilizes METTL3 to promoting HMGB1 degradation to inhibit ferroptosis and enhance gemcitabine resistance in pancreatic cancer.Molecular medicine (Cambridge, Mass.) · 2025Article
- O-GlcNAcylation of glutaminase isoform KGA inhibits ferroptosis through activation of glutaminolysis in hepatoblastoma.Cell death discovery · 2025Article
- Transcriptional Regulators YAP and TAZ Have Distinct Abilities to Compensate for One Another in Podocytes.Journal of the American Society of Nephrology : JASN · 2025Article
- Migrasome Marker Epidermal Growth Factor Domain-SpecificBiomedicines · 2025Article
- Pharmacological Dissection Identifies Retatrutide Overcomes the Therapeutic Barrier of Obese TNBC Treatments through Suppressing the Interplay between Glycosylation and Ubiquitylation of YAP.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- FBXO31-mediated ubiquitination of OGT maintains O-GlcNAcylation homeostasis to restrain endometrial malignancy.Nature communications · 2025Article
- D-ribose-5-phosphate inactivates YAP and functions as a metabolic checkpoint.Journal of hematology & oncology · 2025Article
- Advances in research on the carcinogenic mechanisms and therapeutic potential of YAP1 in bladder cancer (Review).Oncology reports · 2025Review
90 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 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
O-GlcNAcylation has been implicated in the tumorigenesis of various tissue origins, but its function in liver tumorigenesis is not clear. Here, we demonstrate that O-GlcNAcylation can enhance the expression, stability and function of Yes-associated protein (YAP), the downstream transcriptional regulator of the Hippo pathway and a potent oncogenic factor in liver cancer. O-GlcNAcylation induces transformative phenotypes of liver cancer cells in a YAP-dependent manner. An O-GlcNAc site of YAP was identified at Thr241, and mutating this site decreased the O-GlcNAcylation, stability, and pro-tumorigenic capacities of YAP, while increasing YAP phosphorylation. Importantly, we found via in vitro cell-based and in vivo mouse model experiments that O-GlcNAcylation of YAP was required for high-glucose-induced liver tumorigenesis. Interestingly, a positive feedback between YAP and global cellular O-GlcNAcylation is also uncovered. We conclude that YAP O-GlcNAcylation is a potential therapeutic intervention point for treating liver cancer associated with high blood glucose levels and possibly diabetes.
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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.