ArticleOncogene2016
Preventing E-cadherin aberrant N-glycosylation at Asn-554 improves its critical function in gastric cancer.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 130 citations in OpenAlex.
- Context-dependent MAN1A1 protein expression in metastatic breast cancer progression predicts patient survival.BMC cancer · 2025Article
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- Reprogramming CD8+ T-cell Branched N-Glycosylation Limits Exhaustion, Enhancing Cytotoxicity and Tumor Killing.Cancer immunology research · 2025Article
- Glycomics in Human Diseases and Its Emerging Role in Biomarker Discovery.Biomedicines · 2025Review
- Exploring the metabolic signaling network of GFPT in cancer.Cell death discovery · 2025Review
- Glycoproteomics of Gastrointestinal Cancers and Its Use in Clinical Diagnostics.Journal of proteome research · 2025Review
- T-cell branched glycosylation as a mediator of colitis-associated colorectal cancer progression: a potential new risk biomarker in inflammatory bowel disease.Journal of Crohn's & colitis · 2025Article
- Implication of protein post translational modifications in gastric cancer.Frontiers in cell and developmental biology · 2025Review
- Glycosylation in Cancer.Handbook of experimental pharmacology · 2025Review
- The branched N-glycan of PD-L1 predicts immunotherapy responses in patients with recurrent/metastatic HNSCC.Oncogenesis · 2024Article
- Regulation of intracellular activity of N-glycan branching enzymes in mammals.The Journal of biological chemistry · 2024Review
- Decoding the glycoproteome: a new frontier for biomarker discovery in cancer.Journal of hematology & oncology · 2024Review
- Dynamics and functions of E-cadherin complexes in epithelial cell and tissue morphogenesis.Marine life science & technology · 2023Review
- Aberrant N-glycosylation in cancer: MGAT5 and β1,6-GlcNAc branched N-glycans as critical regulators of tumor development and progression.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- Review
- Glucose-mediated N-glycosylation of RPTPα affects its subcellular localization and Src activation.Oncogene · 2023Article
- Decoding TROP2 in breast cancer: significance, clinical implications, and therapeutic advancements.Frontiers in oncology · 2023Review
- Systems-Wide Site-Specific Analysis of Glycoproteins.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Hereditary Diffuse Gastric Cancer: A 2022 Update.Journal of personalized medicine · 2022Review
- Regulation of multiple dimeric states of E-cadherin by adhesion activating antibodies revealed through Cryo-EM and X-ray crystallography.PNAS nexus · 2022Article
8 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
19 authors at 8 institutions in 4 countries.
Funding
Abstract
E-cadherin is a central molecule in the process of gastric carcinogenesis and its posttranslational modifications by N-glycosylation have been described to induce a deleterious effect on cell adhesion associated with tumor cell invasion. However, the role that site-specific glycosylation of E-cadherin has in its defective function in gastric cancer cells needs to be determined. Using transgenic mice models and human clinical samples, we demonstrated that N-acetylglucosaminyltransferase V (GnT-V)-mediated glycosylation causes an abnormal pattern of E-cadherin expression in the gastric mucosa. In vitro models further indicated that, among the four potential N-glycosylation sites of E-cadherin, Asn-554 is the key site that is selectively modified with β1,6 GlcNAc-branched N-glycans catalyzed by GnT-V. This aberrant glycan modification on this specific asparagine site of E-cadherin was demonstrated to affect its critical functions in gastric cancer cells by affecting E-cadherin cellular localization, cis-dimer formation, molecular assembly and stability of the adherens junctions and cell-cell aggregation, which was further observed in human gastric carcinomas. Interestingly, manipulating this site-specific glycosylation, by preventing Asn-554 from receiving the deleterious branched structures, either by a mutation or by silencing GnT-V, resulted in a protective effect on E-cadherin, precluding its functional dysregulation and contributing to tumor suppression.
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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.