ArticleBioMed research international2018
T-Synthase Deficiency Enhances Oncogenic Features in Human Colorectal Cancer Cells via Activation of Epithelial-Mesenchymal Transition.
Article in BioMed research international, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.
- Pooled it
- Bioinformatic Analysis of C1GALT1 in Cancer: Insights Into Prognosis, Metastasis and Therapeutic Potential.Cancer reports (Hoboken, N.J.) · 2025Article
- Tumor-associated Tn and STn antigens: from molecular mechanism to precision diagnosis and treatment.Frontiers in immunology · 2025Review
- Targeting Tn Antigen Suppresses Aberrant O-Glycosylation-Elicited Metastasis in Breast Cancer.Journal of cellular and molecular medicine · 2024Article
- Substrate O-glycosylation actively regulates extracellular proteolysis.Protein science : a publication of the Protein Society · 2024Article
- Review
- Targeting tumor O-glycosylation modulates cancer-immune-cell crosstalk and enhances anti-PD-1 immunotherapy in head and neck cancer.Molecular oncology · 2024Article
- Unraveling the role of C1GALT1 in abnormal glycosylation and colorectal cancer progression.Frontiers in oncology · 2024Review
- ST6GALNAC1 promotes the invasion and migration of breast cancer cells via the EMT pathway.Genes & genomics · 2023Article
- Bittersweet Sugars: How Unusual Glycan Structures May Connect Epithelial-to-Mesenchymal Transition and Multidrug Resistance in Cancer.Medicines (Basel, Switzerland) · 2023Article
- Side population cells derived from hUCMSCs and hPMSCs could inhibit the malignant behaviors of TnStem cell research & therapy · 2023Article
- Association of Glycosylation-Related Genes with Different Patterns of Immune Profiles and Prognosis in Cervical Cancer.Journal of personalized medicine · 2023Article
- The Blessed Union of Glycobiology and Immunology: A Marriage That Worked.Medicines (Basel, Switzerland) · 2023Review
- CD44v6, STn & O-GD2: promising tumor associated antigens paving the way for new targeted cancer therapies.Frontiers in immunology · 2023Review
- A Sweet Warning: Mucin-Type O-Glycans in Cancer.Cells · 2022Review
- Article
- Down-Regulation of C1GALT1 Enhances the Progression of Cholangiocarcinoma through Activation of AKT/ERK Signaling Pathways.Life (Basel, Switzerland) · 2022Article
- C1GALT1 in health and disease.Oncology letters · 2021Review
- Research progress on O-GlcNAcylation in the occurrence, development, and treatment of colorectal cancer.World journal of gastrointestinal surgery · 2021Review
- Glycosylation in Cervical Cancer: New Insights and Clinical Implications.Frontiers in oncology · 2021Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmature truncated O-glycans such as Tn antigen are frequently detected in human colorectal cancer (CRC); however, the precise pathological consequences of Tn antigen expression on CRC are unknown. T-synthase is the key enzyme required for biosynthesis of mature O-glycans. Here we investigated the functional roles of Tn antigen expression mediated by T-synthase deficiency in CRC cells.
methodsTo knock out T-synthase, we used CRISPR-Cas9 technology to target C1GALT1, the gene encoding T-synthase, in a CRC cell line (HCT116). Deletion of T-synthase was confirmed by western blotting, and expression of Tn antigen was determined by flow cytometry in HCT116 cells. We then assessed the biological effects of T-synthase deficiency on oncogenic behaviors in HCT116 cells. Furthermore, we analyzed the mechanistic role of T-synthase deficiency in cancer cells by determining the epithelial-mesenchymal transition (EMT) pathway.
resultsWe showed that forced knockout of T-synthase in HCT116 cells significantly induced Tn antigen expression, which represented the occurrence of aberrant O-glycosylation. Loss of T-synthase significantly enhanced cell proliferation and adhesion, as well as migration and invasiveness in culture. More importantly, we demonstrated that T-synthase deficiency directly induced classical EMT characteristics in cancer cells. E-cadherin, a typical epithelial cell marker, was markedly decreased in T-synthase knockout HCT 116 cells, accompanied by an enhanced expression of mesenchymal markers including snail and fibronectin (FN).
conclusionsThese findings indicate that T-synthase deficiency in CRC cells not only is responsible for aberrant O-glycosylation, but also triggers the molecular process of EMT pathway, which may translate to increased invasiveness and metastasis in cancers.
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