ArticleBritish journal of cancer2013
Human fucosyltransferase 6 enables prostate cancer metastasis to bone.
Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
- The glycobiology of prostate cancer: an update.Oncogene · 2026Review
- Dynamic Shifts in ER-Plasma Membrane Junctions Signaling Define Pro-Metastatic N-Glycosylation and Predict Prostate Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Structure, function, and implications of fucosyltransferases in health and disease.Nature communications · 2025Review
- Realizing the promise of 'La Dolce Vita' via chemical biology: glycan-motif editing of sLeThe FEBS journal · 2025Review
- FUT8 Is a Critical Driver of Prostate Tumour Growth and Can Be Targeted Using Fucosylation Inhibitors.Cancer medicine · 2025Article
- Targeted inhibition of ferroptosis in bone marrow mesenchymal stem cells by engineered exosomes alleviates bone loss in smoking-related osteoporosis.Materials today. Bio · 2025Article
- Prostate Cancer Bone Metastasis: Molecular Mechanisms of Tumor and Bone Microenvironment.Cancer management and research · 2025Review
- A functional variant rs10409772 in FUT6 promoter regulates colorectal cancer progression through PKA/CREB signaling.Translational oncology · 2024Article
- The role ofActa pharmaceutica Sinica. B · 2024Review
- Harnessing upregulated E-selectin while enhancing SDF-1α sensing redirects infused NK cells to the AML-perturbed bone marrow.Leukemia · 2024Article
- Targeting aberrant sialylation and fucosylation in prostate cancer cells using potent metabolic inhibitors.Glycobiology · 2023Article
- MDA-9/Syntenin in the tumor and microenvironment defines prostate cancer bone metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Elevation of α-1,3 fucosylation promotes the binding ability of TNFR1 to TNF-α and contributes to osteoarthritic cartilage destruction and apoptosis.Arthritis research & therapy · 2022Article
- Major differences in glycosylation and fucosyltransferase expression in low-grade versus high-grade bladder cancer cell lines.Glycobiology · 2021Article
- Review
- Mass Spectrometry-Based Glycoproteomics and Prostate Cancer.International journal of molecular sciences · 2021Review
- Narrative review of urinary glycan biomarkers in prostate cancer.Translational andrology and urology · 2021Review
- Post-Translational Modifications That Drive Prostate Cancer Progression.Biomolecules · 2021Review
- Altered mRNA Expression of Fucosyltransferases and Fucosidase Predicts Prognosis in Human Oral Carcinoma.International journal of molecular and cellular medicine · 2021Article
- Lectin drug conjugate therapy for colorectal cancer.Cancer science · 2020Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe interaction between human prostate cancer (PCa) cells and bone marrow (BM) endothelium follows a rolling-and-adhesion cascade mediated by E-selectin ligand (ESL): E-selectin. This adhesion is enabled by elevated expression of α-1,3-fucosyltransferases (FTs), enzymes responsible for ESL-mediated bone metastasis in humans. In contrast, the incidence of bone metastasis in mice is rare.
methodsFT 3, 6 and 7 were overexpressed in mouse PCa cells. The rolling cell number, cell-rolling velocity and transendothelial migration were characterised in vitro. Fucosyltransferases-transduced mouse PCa cells expressing luciferase were inoculated into mice via left ventricle to compare the capability of bone metastasis. Mass spectrometry and immunoprecipitation were utilised for identification of ESLs.
resultsOverexpression of FT3, FT6 or FT7 restored ESLs and enabled mouse PCa cells to roll and adhere in E-selectin-functionalised microtubes, similar to trafficking of circulating PCa cells in BM vessels. Following intracardiac inoculation, FT6-transduced cells induced robust bone metastasis in mice. Inhibition of FT6 by a fucose mimetic significantly reduced bone metastasis. Importantly, comparison of FT3, FT6 and FT7 gene expression in existing clinical samples showed significant upregulation of FT6 in PCa-distant metastases.
conclusionFT6 is a key mediator of PCa cells trafficking to the BM. It may serve as a viable drug target in preclinical tests of therapeutics for reduction of PCa bone metastasis.
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