ArticleGenes & genomics2023
ST6GALNAC1 promotes the invasion and migration of breast cancer cells via the EMT pathway.
Article in Genes & genomics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Targeting Siglec-engaging immunosuppressive sialoglycans to suppress prostate cancer bone metastasis.British journal of cancer · 2026Article
- Targeting sialic acid metabolism: a therapeutic strategy against gastric cancer driven by WZ35.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Writers and readers of sialylation in immunoregulation in cancer.The Journal of biological chemistry · 2026Review
- Sialylation in Thyroid Carcinoma: An Overview of Mechanisms, Markers, and Therapeutic Opportunities.Journal of Cancer · 2026Review
- Dysregulated Sialylation in Cancer: From Immunosuppressive Microenvironment to Siglec-Targeted Therapeutics.Biomolecules · 2025Review
- ST6GALNAC1 mediates sialylation of mucins in non-small cell lung cancer to evade immune surveillance.Journal of thoracic disease · 2025Article
- Integrated tumour-immune cell response modelling of luminal a breast cancer details malignant signalling and ST3Gal1 inhibitor-induced reversal.Glycobiology · 2025Article
- Association of Gene Expression Profiles in HPV-Positive Head and Neck Squamous Cell Carcinoma with Patient Outcome: In Search of Prognostic Biomarkers.International journal of molecular sciences · 2025Article
- Charge matters: how flanking substrate charge modulates O-glycan Core elongation.Glycobiology · 2025Article
- Article
- When a negative (charge) is not a positive: sialylation and its role in cancer mechanics and progression.Frontiers in oncology · 2024Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA specific sialyl-transferases called ST6GALNAC1 has been proven to up-regulate abnormal O-glycosylation, which is strongly associated with tumorigenesis and cancer progression. However, the precise pathological outcome of ST6GALNAC1 expression in breast cancer cells remains unknown. Therefore, our study aims to investigate the functional role of ST6GALNAC1 and its impact on the epithelial-mesenchymal transition (EMT) pathway in breast cancer cells.
methodsPlasmids with siRNA were used to construct ST6GALNAC1 knockoff (si-ST6GALNAC1) MDA-MB-231 and MDA-MB-453 cells, while lentiviruses were used to construct ST6GALNAC1 over-expression (oe-ST6GALNAC1) MCF-7 and BT474 cells. Transfer efficiency was verified by Western Blot. Then we selected transfected cells and assessed the changes in cell proliferation, invasion, migration, and EMT markers.
resultsThe expression of ST6GALNAC1 significantly enhanced cell migration and invasion, which was confirmed by Wound Scratch Assay and Transwell Assay. Particularly, ST6GALNAC1 expression directly induced the EMT signaling pathway. E-cadherin was markedly decreased in oe-ST6GALNAC1 cells, accompanied by an up-regulation of mesenchymal markers including N-cadherin, snail, and ZEB1. However, no significant correlation was found between ST6GALNAC1 expression and cell proliferation. All of the outcomes were reversely validated in si-ST6GALNAC1 cells.
conclusionsThe expression of ST6GALNAC1 promotes cell migration and invasion probably by triggering the molecular process of the EMT pathway in breast cancer cells, which may provide new clues for designing novel molecular targeted drugs in breast cancer treatment.
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