ArticleJCI insight2024
N-glycosylation by Mgat5 imposes a targetable constraint on immune-mediated tumor clearance.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Genetic and biochemical screens identify MGAT1 as a druggable glycosyltransferase target in STK11-mutant lung cancer.The Journal of biological chemistry · 2026Article
- Immune implications and therapeutic opportunities of tumor glycosylation.Nature cancer · 2026Review
- Co-repression of Yap1 and Sox9 abrogates established cholangiocarcinoma by eliminating transcriptional compensation.Clinical and molecular hepatology · 2026Article
- Co-repression ofbioRxiv : the preprint server for biology · 2026Article
- Epigenetic and metabolic plasticity of tumor cells in immunotherapy resistance.Frontiers in immunology · 2026Review
- Glycan-encoded immune checkpoints and allorecognition: a mechanistic framework for transplantation and organ engineering.Frontiers in transplantation · 2026Review
- Tuning CAR-T cells by targeting cancer-associated glycan in pancreatic cancer.Nature communications · 2025Article
- Glycosylation in cancer: mechanisms, diagnostic markers, and therapeutic applications.Molecular and cellular biochemistry · 2025Review
- Targeting protein modification: a new direction for immunotherapy of pancreatic cancer.International journal of biological sciences · 2025Review
- Clonal divergence and genomic meltdown in prostatic pleomorphic giant cell adenocarcinoma.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
The regulated glycosylation of the proteome has widespread effects on biological processes that cancer cells can exploit. Expression of N-acetylglucosaminyltransferase V (encoded by Mgat5 or GnT-V), which catalyzes the addition of β1,6-linked N-acetylglucosamine to form complex N-glycans, has been linked to tumor growth and metastasis across tumor types. Using a panel of murine pancreatic ductal adenocarcinoma (PDAC) clonal cell lines that recapitulate the immune heterogeneity of PDAC, we found that Mgat5 is required for tumor growth in vivo but not in vitro. Loss of Mgat5 results in tumor clearance that is dependent on T cells and dendritic cells, with NK cells playing an early role. Analysis of extrinsic cell death pathways revealed Mgat5-deficient cells have increased sensitivity to cell death mediated by the TNF superfamily, a property that was shared with other non-PDAC Mgat5-deficient cell lines. Finally, Mgat5 knockout in an immunotherapy-resistant PDAC line significantly decreased tumor growth and increased survival upon immune checkpoint blockade. These findings demonstrate a role for N-glycosylation in regulating the sensitivity of cancer cells to T cell killing through classical cell death pathways.
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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.