ArticleThe EMBO journal2011
A novel strategy for evasion of NK cell immunity by tumours expressing core2 O-glycans.
Article in The EMBO journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
84 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.
- Pooled it
- Differential expression patterns of N-acetylglucosaminyl transferases and polylactosamines in uterine lesions.European journal of histochemistry : EJH · 2014Trial
- Engineering immune cell engagers: From molecular constructs to biomaterial platforms.Materials today. Bio · 2026Review
- Tumor glycosylation and ABO phenotyping alterations in invasive urothelial carcinoma: A case report.Hematology, transfusion and cell therapy · 2026Article
- Harnessing the potential of γδ T cells through engineering and combination treatment for cancer therapies.Nature communications · 2026Review
- Galectin-3 Release in the Bone Marrow Microenvironment Promotes Drug Resistance and Relapse in Acute Myeloid Leukemia.Life (Basel, Switzerland) · 2025Review
- Glycosphingolipids as emerging attack points in bladder cancer.Discover oncology · 2025Review
- Multifaceted roles of Galectins: from carbohydrate binding to targeted cancer therapy.Biomarker research · 2025Review
- Low GCNT2/I-Branching Glycan Expression Is Associated with Bladder Cancer Aggressiveness.Biomedicines · 2025Article
- Collagen Mineralization Decreases NK Cell-Mediated Cytotoxicity of Breast Cancer Cells via Increased Glycocalyx Thickness.Advanced materials (Deerfield Beach, Fla.) · 2024Article
- Article
- Immunoengineering can overcome the glycocalyx armour of cancer cells.Nature materials · 2024Article
- Galectin-3 and cancer immunotherapy: a glycobiological rationale to overcome tumor immune escape.Journal of experimental & clinical cancer research : CR · 2024Article
- COLLAGEN MINERALIZATION DECREASES NK CELL-MEDIATED CYTOTOXICITY OF BREAST CANCER CELLS VIA INCREASED GLYCOCALYX THICKNESS.bioRxiv : the preprint server for biology · 2024Article
- Elevated Galectin-3 levels in the tumor microenvironment of ovarian cancer - implication of ROS mediated suppression of NK cell antitumor response via tumor-associated neutrophils.Frontiers in immunology · 2024Article
- The role of GCNT1 mediated O-glycosylation in aggressive prostate cancer.Scientific reports · 2023Article
- Role of TruncatedCancers · 2023Review
- Altered Glycosylation in Progression and Management of Bladder Cancer.Molecules (Basel, Switzerland) · 2023Review
- Expression and localisation of MUC1 modified with sialylated core-2 O-glycans in mucoepidermoid carcinoma.Scientific reports · 2023Article
- Vdelta1 T cells are more resistant than Vdelta2 T cells to the immunosuppressive properties of galectin-3.Frontiers in immunology · 2023Article
24 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
16 authors at 4 institutions in 4 countries.
Funding
Abstract
The O-glycan branching enzyme, core2 β-1,6-N-acetylglucosaminyltransferase (C2GnT), forms O-glycans containing an N-acetylglucosamine branch connected to N-acetylgalactosamine (core2 O-glycans) on cell-surface glycoproteins. Here, we report that upregulation of C2GnT is closely correlated with progression of bladder tumours and that C2GnT-expressing bladder tumours use a novel strategy to increase their metastatic potential. Our results showed that C2GnT-expressing bladder tumour cells are highly metastatic due to their high ability to evade NK cell immunity and revealed the molecular mechanism of the immune evasion by C2GnT expression. Engagement of an NK-activating receptor, NKG2D, by its tumour-associated ligand, Major histocompatibility complex class I-related chain A (MICA), is critical to tumour rejection by NK cells. In C2GnT-expressing bladder tumour cells, poly-N-acetyllactosamine was present on core2 O-glycans on MICA, and galectin-3 bound the NKG2D-binding site of MICA through this poly-N-acetyllactosamine. Galectin-3 reduced the affinity of MICA for NKG2D, thereby severely impairing NK cell activation and silencing the NK cells. This new mode of NK cell silencing promotes immune evasion of C2GnT-expressing bladder tumour cells, resulting in tumour metastasis.
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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.