ArticleCell death & disease2023
C1GalT1 expression reciprocally controls tumour cell-cell and tumour-macrophage interactions mediated by galectin-3 and MGL with double impact on cancer development and progression.
Article in Cell death & disease, 2023. 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, 13 citations in OpenAlex.
- Immunotherapy impact of macrophage glycosylation on cholangiocarcinoma and its prognostic and immune microenvironment significance.Human vaccines & immunotherapeutics · 2026Article
- Targeting galectin-3 in cancer by novel and unique inhibitors of non-carbohydrate origin.Molecular medicine (Cambridge, Mass.) · 2025Article
- Bioinformatic Analysis of C1GALT1 in Cancer: Insights Into Prognosis, Metastasis and Therapeutic Potential.Cancer reports (Hoboken, N.J.) · 2025Article
- Tumor-secreted galectin-3 suppresses antitumor response by inducing IL-10Journal for immunotherapy of cancer · 2025Article
- The macrophage galactose-type C-type lectin 1 receptor plays a major role in mediating colitis-associated colorectal cancer malignancy.Immunology and cell biology · 2025Article
- Sugar symphony: glycosylation in cancer metabolism and stemness.Trends in cell biology · 2025Review
- The role of glycan-lectin interactions in the tumor microenvironment: immunosuppression regulators of colorectal cancer.American journal of cancer research · 2025Review
- C1GALT1 induces the carcinogenesis of thyroid cancer through regulation by miR-141-3p and GLUT1.Heliyon · 2024Article
- High core 1β1,3-galactosyltransferase 1 expression is associated with poor prognosis and promotes cellular radioresistance in lung adenocarcinoma.Journal of cancer research and clinical oncology · 2024Article
- Unraveling the role of C1GALT1 in abnormal glycosylation and colorectal cancer progression.Frontiers in oncology · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although most cell membrane proteins are modified by glycosylation, our understanding of the role and actions of protein glycosylation is still very limited. β1,3galactosyltransferase (C1GalT1) is a key glycosyltransferase that controls the biosynthesis of the Core 1 structure of O-linked mucin type glycans and is overexpressed by many common types of epithelial cancers. This study reports that suppression of C1GalT1 expression in human colon cancer cells caused substantial changes of protein glycosylation of cell membrane proteins, many of which were ligands of the galactoside-binding galectin-3 and the macrophage galactose-type lectin (MGL). This led to significant reduction of cancer cell proliferation, adhesion, migration and the ability of tumour cells to form colonies. Crucially, C1GalT1 suppression significantly reduced galectin-3-mediated tumour cell-cell interaction and galectin-3-promoted tumour cell activities. In the meantime, C1GalT1 suppression substantially increased MGL-mediated macrophage-tumour cell interaction and macrophage-tumour cell phagocytosis and cytokine secretion. C1GalT1-expressing cancer cells implanted in chick embryos resulted in the formation of significantly bigger tumours than C1GalT1-suppressed cells and the presence of galectin-3 increased tumour growth of C1GalT1-expressing but not C1GalT1-suppressed cells. More MGL-expressing macrophages and dendritic cells were seen to be attracted to the tumour microenvironment in ME C1galt1
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