ArticleJournal of neuro-oncology2019
Fucosyltransferase 4 and 7 mediates adhesion of non-small cell lung cancer cells to brain-derived endothelial cells and results in modification of the blood-brain-barrier: in vitro investigation of CD15 and CD15s in lung-to-brain metastasis.
Article in Journal of neuro-oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 48 citations in OpenAlex.
- L-Fucose: a dietary sugar with multifaceted potential in the biology and therapy of cancer.Nature reviews. Cancer · 2026Review
- Fucosyltransferase 4-derived peptide bioconjugates on carbon nanotubes enhance antitumor immunity in an ovarian cancer mouse model.Frontiers in immunology · 2026Article
- Structure, function, and implications of fucosyltransferases in health and disease.Nature communications · 2025Review
- Blood-brain barrier alterations as an initiator of brain metastasis from lung cancer: a new take on an old story.Cancer gene therapy · 2025Review
- Integration of RNAseq transcriptomics andChemical science · 2025Article
- Immune genes involved in synaptic plasticity during early postnatal brain development contribute to post-stroke damage in the aging male rat brain.Biogerontology · 2025Article
- Exosome-based targeted delivery of NF-κB ameliorates age-related neuroinflammation in the aged mouse brain.Experimental & molecular medicine · 2025Article
- MicroRNAs in Lung Cancer Brain Metastasis.International journal of molecular sciences · 2024Review
- Altered expression of Sialyl Lewis X in experimental models of Parkinson's disease.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Androgen drives melanoma invasiveness and metastatic spread by inducing tumorigenic fucosylation.Nature communications · 2024Article
- Fucosyltransferase 3 and 8 promote the metastatic capacity of cancer stem-like cells via CD15s and E-cadherin in esophageal cancer.Iranian journal of basic medical sciences · 2024Article
- The origin of brain malignancies at the blood-brain barrier.Cellular and molecular life sciences : CMLS · 2023Review
- Review
- FUT2 inhibits the EMT and metastasis of colorectal cancer by increasing LRP1 fucosylation.Cell communication and signaling : CCS · 2023Article
- Targeting protein glycosylation to regulate inflammation in the respiratory tract: novel diagnostic and therapeutic candidates for chronic respiratory diseases.Frontiers in immunology · 2023Review
- Novel blood-based FUT7 DNA methylation is associated with lung cancer: especially for lung squamous cell carcinoma.Clinical epigenetics · 2022Article
- Review
- Review
- Glycosylation as a regulator of site-specific metastasis.Cancer metastasis reviews · 2022Review
- Aberrant Protein Glycosylation in Brain Cancers, with Emphasis on Glioblastoma.Advances in experimental medicine and biology · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMetastatic non-small cell lung (NSCLC) cancer represents one of the most common types of brain metastasis. The mechanisms involved in how circulating cancer cells transmigrate into brain parenchyma are not fully understood. The aim of this work was to investigate the role of fucosylated carbohydrate epitopes CD15 and sialyated CD15s in cancer adhesion to brain-derived endothelial cells and determine their influence in blood-brain barrier (BBB) disruption
methodsThree distinct, independent methods were used to measure brain endothelial integrity and include voltohmmeter (EVOM™), impedance spectroscopy (CellZscope®) and electric cell-substrate impedance sensing system (ECIS™). Two fucosyltransferases (FUT4 and 7) responsible for CD15 and CD15s synthesis were modulated in four human cancer cell lines (three lung cancer and one glioma).
resultsOverexpression of CD15 or CD15s epitopes led to increase in adhesion of cancer cells to cerebral endothelial cells compared with wild-type and cells with silenced CD15 or CD15s (p < 0.01). This overexpression led to the disruption of cerebral endothelial cell monolayers (p < 0.01). Knockdown of FUT4 and FUT7 in metastatic cancer cells prevented disruption of an in vitro BBB model. Surprisingly, although the cells characterised as 'non-metastatic', they became 'metastatic' -like when cells were forced to over-express either FUT4 or FUT7.
conclusionsResults from these studies suggest that overexpression of CD15 and CD15s could potentiate the transmigration of circulating NSCLC cells into the brain. The clinical significance of these studies includes the possible use of these epitopes as biomarkers for metastasis.
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