ArticleCellular oncology (Dordrecht, Netherlands)2025
ST6GAL1-mediated sialylation inhibits the antitumor immune response in colorectal cancer.
Article in Cellular oncology (Dordrecht, Netherlands), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Inhibition of Aurora B induces senescence and potentiates immunotherapy in hepatocellular carcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Distinct clinical and genomic profiles of braf mutation subtypes in Chinese colorectal cancer: a retrospective cohort study with cross-population validation.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Shared glycosylation-related molecular mechanism and immune infiltration patterns of fetal growth restriction and preeclampsia.Frontiers in immunology · 2026Article
- Enhanced sialylation of bone marrow mesenchymal stromal cells contributes to immune remodeling through macrophage polarization in multiple myeloma patients.Frontiers in immunology · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
purposeInterferon gamma (IFNG) directly affects the antitumor immune response. ST6-β-galactoside α-2,6-sialyltransferase 1 (ST6GAL1) is also positively correlated with poor prognosis for colorectal cancer (CRC). we performed some works to exploreexplored the underlying mechanism to further understand immune escape in colorectal cancer (CRC).
methodsFirst, we used clinical samples to confirm the relationship between ST6GAL1 and CRC. Afterward, we constructed overexpression/knockdown cell lines and performed bulk RNA sequencing, kinase phosphorylation chip, mass spectrometry, and in vitro and in vivo assays to explore the mechanism regulated by ST6GAL1. Finally, we verified the mechanism by performing immunoprecipitation and immunofluorescence (IF) staining.
resultsST6-β-galactoside α-2,6-sialyltransferase 1 (ST6GAL1) expression was negatively correlated with the response to neoadjuvant chemotherapy in patients with CRC and negatively correlated with the sensitivity to IFNG in CRC cell lines. We confirmed that ST6GAL1 overexpression inhibited the infiltration of effector T cells, the levels of IFNG produced by CD8
conclusionsOur results confirmed that ST6GAL1 decreases the sensitivity of tumor cells to IFNG. This study describes a novel mechanism by which ST6GAL1 promotes the immune escape and malignant progression of CRC.
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