ArticleAngiogenesis2024
Sialyl Lewis X decorated integrin α3 on small extracellular vesicles promotes metastasis of bladder cancer via enhancing vascular permeability.
Article in Angiogenesis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- Aberrant fucosylation of extracellular vesicles remodels the vascular microenvironment and promotes chemoresistance in myelodysplastic syndromes and acute myeloid leukemia.Haematologica · 2026Article
- O-GlcNAcylated TAP1 Impairs Antigen Presentation and Promotes Immune Evasion in Bladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The 'sugar' side of extracellular vesicle-glycome: a panorama from basic characteristics, deciphering technologies, functions, to applications.Journal of nanobiotechnology · 2026Review
- Adhesion to aggression: unravelling sLeClinical & experimental metastasis · 2025Review
- Glycomics in Human Diseases and Its Emerging Role in Biomarker Discovery.Biomedicines · 2025Review
- Realizing the promise of 'La Dolce Vita' via chemical biology: glycan-motif editing of sLeThe FEBS journal · 2025Review
- Integrated muti-omics data and machine learning reveal CD151 as a key biomarker inducing chemoresistance in metabolic syndrome-related early-onset left-sided colorectal cancer.Functional & integrative genomics · 2025Article
- Bisecting GlcNAc modification of vesicular GAS6 regulates CAFs activation and breast cancer metastasis.Cell communication and signaling : CCS · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
The permeability of blood vessels plays a crucial role in the spread of cancer cells, facilitating their metastasis at distant sites. Small extracellular vesicles (sEVs) are known to contribute to the metastasis of various cancers by crossing the blood vessel wall. However, the role of abnormal glycoconjugates on sEVs in tumor blood vessels remains unclear. Our study found elevated levels of fucosyltransferase VII (FUT7) and its product sialyl Lewis X (sLeX) in muscle-invasive bladder cancer (BLCA), with high levels of sLeX promoting the growth and invasion of BLCA cells. Further investigation revealed that sLeX was enriched in sEVs derived from BLCA. sLeX-decorated sEVs increased blood vessel permeability by disrupting the tight junctions of human umbilical vein endothelial cells (HUVECs). Using the glycoproteomics approach, we identified integrin α3 (ITGA3) as a sLeX-bearing glycoprotein in BLCA cells and their sEVs. Mechanically, sLeX modification stabilized ITGA3 by preventing its degradation in lysosomes. sEVs carrying sLeX-modified ITGA3 can be effectively internalized by HUVECs, leading to a decrease in the expression of tight junction protein. Conversely, silencing ITGA3 in sLeX-decorated sEVs restored tight junction proteins and reduced blood vessel permeability by inhibiting the MAPK pathway. Moreover, sLeX-modification of ITGA3 at Asn 265 in HUVECs promoted occludin dephosphorylation at Ser/Thr residues, followed by inducing its importin α1-mediated nuclear translocation, which resulted in the disruption of tight junctions. Our findings suggest a potential strategy for disrupting the formation of a metastatic microenvironment and preventing the spread of malignant bladder cancer.
Indexed as
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Registered trials
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