ArticleThe Journal of biological chemistry2014
β-Galactoside α2,6-sialyltranferase 1 promotes transforming growth factor-β-mediated epithelial-mesenchymal transition.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 112 citations in OpenAlex.
- Galectin-3 Mediates TGF-β-Controlled Migration in Müller Glial Cells.International journal of molecular sciences · 2026Article
- Dose-Dependent Inhibition of Protein Glycosylation Reveals Crosstalk between Glycosylation and Phosphorylation in EGF Signaling Pathways.Analytical chemistry · 2026Article
- Downregulation of sialyl-transferases and their role in malignant meningioma cells.Biomedical reports · 2026Article
- Novel lithocholic acid-diindolylmethane hybrids as potent sialyltransferase inhibitors targeting triple-negative breast cancer: a molecular hybridization approach.RSC medicinal chemistry · 2025Article
- Multi-omics reveals that ST6GAL1 promotes colorectal cancer progression through LGALS3BP sialylation.Biomolecules & biomedicine · 2025Article
- Machine learning-based integration identifies plasma cells-related gene signature ST6GAL1 in idiopathic pulmonary fibrosis.BMC pulmonary medicine · 2025Article
- Black rice bran‑derived anthocyanins attenuate cholangiocarcinoma cell migration via the alteration of epithelial‑mesenchymal transition and sialylation.Biomedical reports · 2025Article
- ST6GAL1 Promotes Epithelial-to-Mesenchymal Transition in Breast Cancer via the HIF-HK2 Signaling Pathway.Breast cancer (Dove Medical Press) · 2025Article
- Glycosylation: mechanisms, biological functions and clinical implications.Signal transduction and targeted therapy · 2024Review
- Sialic acid in the regulation of blood cell production, differentiation and turnover.Immunology · 2024Review
- Specific sialylation of N-glycans and its novel regulatory mechanism.Glycoconjugate journal · 2024Review
- Role of ST6GAL1 in Thyroid Cancers: Insights from Tissue Analysis and Genomic Datasets.International journal of molecular sciences · 2023Article
- ST6GAL1 sialyltransferase promotes acinar to ductal metaplasia and pancreatic cancer progression.JCI insight · 2023Article
- ST6GAL1 inhibits metastasis of hepatocellular carcinoma via modulating sialylation of MCAM on cell surface.Oncogene · 2023Article
- Glycosylation Alterations in Cancer Cells, Prognostic Value of Glycan Biomarkers and Their Potential as Novel Therapeutic Targets in Breast Cancer.Biomedicines · 2022Review
- Review
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- Glycosylation as a regulator of site-specific metastasis.Cancer metastasis reviews · 2022Review
- Biosynthesis and Biological Significances of LacdiNAc Group onBiomolecules · 2022Review
- Long noncoding RNA TINCR facilitates hepatocellular carcinoma progression and dampens chemosensitivity to oxaliplatin by regulating the miR-195-3p/ST6GAL1/NF-κB pathway.Journal of experimental & clinical cancer research : CR · 2022Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
β-Galactoside α2,6-sialyltranferase 1 (ST6GAL1) catalyzes the addition of terminal α2,6-sialylation to N-glycans. Increased expression of ST6GAL1 has been reported in diverse carcinomas and highly correlates with tumor progression. Here, we report that St6gal1 transcription and α2,6-sialylated N-glycans are up-regulated during TGF-β-induced epithelial-mesenchymal transition (EMT) in GE11 cells, requiring the Sp1 element within the St6gal1 promoter. Knockdown of St6gal1 strongly suppressed TGF-β-induced EMT with a concomitant increase in E-cadherin expression, a major determinant of epithelial cell adherens junctions. Conversely, overexpression of ST6GAL1 increased the turnover of cell surface E-cadherin and promoted TGF-β-induced EMT. Overexpressing β-galactoside α2,3-sialyltranferase 4 had little influence on EMT, indicating specificity for α2,6-sialylation. The basal mesenchymal phenotype of MDA-MB-231 human breast cancer cells was partially reversed by ST6GAL1 silencing. Moreover, ST6GAL1 knockdown inhibited the phosphorylation of Akt, but not Smad2, suggesting that ST6GAL1 contributes to EMT through a non-Smad signaling pathway. Taken together, our data indicate that ST6GAL1 promotes TGF-β-dependent EMT as well as maintenance of the mesenchymal state by growth signaling, providing a plausible mechanism whereby up-regulated ST6GAL1 may promote malignant progression.
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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.