ArticleOncology reports2013
Suppression of FUT1 attenuates cell proliferation in the HER2-overexpressing cancer cell line NCI-N87.
Article in Oncology reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 32 citations in OpenAlex.
- Structure, function, and implications of fucosyltransferases in health and disease.Nature communications · 2025Review
- H Antigen expression modulates epidermal Keratinocyte Integrity and differentiation.Biological research · 2024Article
- Investigation of the impact of Globo-H expression on the progression of gastric cancer.American journal of cancer research · 2023Article
- Aberrant Fucosylation of Saliva Glycoprotein Defining Lung Adenocarcinomas Malignancy.ACS omega · 2022Article
- A Novel Bispecific Antibody Targeting CD3 and Lewis Y with Potent Therapeutic Efficacy against Gastric Cancer.Biomedicines · 2021Article
- Role of Glycans on Key Cell Surface Receptors That Regulate Cell Proliferation and Cell Death.Cells · 2021Review
- TUG1 knockdown promoted viability and inhibited apoptosis and cartilage ECM degradation in chondrocytes via the miR-17-5p/FUT1 pathway in osteoarthritis.Experimental and therapeutic medicine · 2020Article
- Terminal fucose mediates progression of human cholangiocarcinoma through EGF/EGFR activation and the Akt/Erk signaling pathway.Scientific reports · 2019Article
- Article
- HIT000218960 promotes gastric cancer cell proliferation and migration through upregulation of HMGA2 expression.Oncology letters · 2019Article
- Fucosyltransferase 1 and 2 play pivotal roles in breast cancer cells.Cell death discovery · 2019Article
- Inhibition of fucosylation in human invasive ductal carcinoma reduces E-selectin ligand expression, cell proliferation, and ERK1/2 and p38 MAPK activation.Molecular oncology · 2018Article
- Glycosylation as a Main Regulator of Growth and Death Factor Receptors Signaling.International journal of molecular sciences · 2018Review
- c-Fos mediates α1, 2-fucosyltransferase 1 and Lewis y expression in response to TGF-β1 in ovarian cancer.Oncology reports · 2017Article
- miR-200b inhibits proliferation and metastasis of breast cancer by targeting fucosyltransferase IV and α1,3-fucosylated glycans.Oncogenesis · 2017Article
- Fucosylation of LAMP-1 and LAMP-2 by FUT1 correlates with lysosomal positioning and autophagic flux of breast cancer cells.Cell death & disease · 2016Article
- The role of the histoblood ABO group in cancer.Future science OA · 2016Review
- New NCI-N87-derived human gastric epithelial line after human telomerase catalytic subunit over-expression.World journal of gastroenterology · 2015Article
- Synthesis and cell-selective antitumor properties of amino acid conjugated tumor-associated carbohydrate antigen-coated gold nanoparticles.Carbohydrate research · 2015Article
- Biosynthetic Machinery Involved in Aberrant Glycosylation: Promising Targets for Developing of Drugs Against Cancer.Frontiers in oncology · 2015Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lewis Y (LeY) antigen is an oligosaccharide that is highly expressed at the cell surface in various human cancers. Increased LeY expression activates epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) and promotes cell proliferation in EGFR-overexpressing cells. However, the effect of downregulation of LeY expression on cell proliferation in HER2-overexpressing cells remains unknown. FUT1 encodes α1,2-fucosyltransferase, a key enzyme for LeY synthesis. We knocked down FUT1 by short interfering RNA (siRNA) in four HER2-overexpressing human cancer cell lines, including NCI-N87, MKN7, SKBr3 and BT474. We investigated whether downregulation of LeY and alteration in the glycosylation status of these cells affect cell proliferation and HER2 activation. Knocking down FUT1 expression markedly inhibited proliferation of NCI-N87, which highly expressed EGFR and was sensitive to EGFR deprivation. Furthermore, FUT1 siRNA downregulated the total amount of HER2 protein, phosphorylation of HER2 and EGFR, and phosphorylation of extracellular signal-regulated kinase (ERK) in this cell line. Moreover, the marked downregulation of phosphorylation of HER2 and ERK was observed following short-time EGF-stimulation. These effects were not observed in the other three cell lines. Our results suggest that knockdown of FUT1 downregulates HER2 signaling via EGFR downregulation. FUT1 may serve as a new molecular target for HER2-overexpressing human cancers with activated EGFR signaling.
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