ArticleThe Journal of biological chemistry2008
The proteoglycan brevican binds to fibronectin after proteolytic cleavage and promotes glioma cell motility.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 98 citations in OpenAlex.
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- Activity-dependent extracellular proteolytic cascade cleaves the ECM component brevican to promote structural plasticity.EMBO reports · 2026Article
- Extracellular matrix stiffness conditions glioblastoma cells for long-term migration: Mechanical memory as a driver of invasion and recurrence in glioblastoma.Neuro-oncology · 2026Review
- Defining the extracellular matrix for targeted immunotherapy in adult and pediatric brain cancer.NPJ precision oncology · 2025Article
- O-GalNAc glycans are enriched in neuronal tracts and regulate nodes of Ranvier.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Recent Developments in Glioblastoma-On-A-Chip for Advanced Drug Screening Applications.Small (Weinheim an der Bergstrasse, Germany) · 2025Review
- Review
- CHST11-modified chondroitin 4-sulfate as a potential therapeutic target for glioblastoma.American journal of cancer research · 2023Article
- Laminin-5, Fibronectin, and Type IV Collagen as Potential Biomarkers of Brain Glioma Malignancy.Biomedicines · 2022Article
- Proteolysis: a key post-translational modification regulating proteoglycans.American journal of physiology. Cell physiology · 2022Review
- A Tumor-Homing Peptide Platform Enhances Drug Solubility, Improves Blood-Brain Barrier Permeability and Targets Glioblastoma.Cancers · 2022Article
- Glycomaterials to Investigate the Functional Role of Aberrant Glycosylation in Glioblastoma.Advanced healthcare materials · 2022Review
- On-tissue spatially resolved glycoproteomics guided by N-glycan imaging reveal global dysregulation of canine glioma glycoproteomic landscape.Cell chemical biology · 2022Article
- Advanced quantification for single-cell adhesion by variable-angle TIRF nanoscopy.Biophysical reports · 2021Article
- Progress in mimicking brain microenvironments to understand and treat neurological disorders.APL bioengineering · 2021Article
- Targeting glioblastoma using a novel peptide specific to a deglycosylated isoform of brevican.Advanced therapeutics · 2021Article
- ADAMTS proteases and the tumor immune microenvironment: Lessons from substrates and pathologies.Matrix biology plus · 2021Review
- Synthesis and Screening of α-Xylosides in Human Glioblastoma Cells.Molecular pharmaceutics · 2021Article
- Mechanisms of Invasion in Glioblastoma: Extracellular Matrix, CaFrontiers in cellular neuroscience · 2021Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The adult neural parenchyma contains a distinctive extracellular matrix that acts as a barrier to cell and neurite motility. Nonneural tumors that metastasize to the central nervous system almost never infiltrate it and instead displace the neural tissue as they grow. In contrast, invasive gliomas disrupt the extracellular matrix and disperse within the neural tissue. A major inhibitory component of the neural matrix is the lectican family of chondroitin sulfate proteoglycans, of which brevican is the most abundant member in the adult brain. Interestingly, brevican is also highly up-regulated in gliomas and promotes glioma dispersion by unknown mechanisms. Here we show that brevican secreted by glioma cells enhances cell adhesion and motility only after proteolytic cleavage. At the molecular level, brevican promotes epidermal growth factor receptor activation, increases the expression of cell adhesion molecules, and promotes the secretion of fibronectin and accumulation of fibronectin microfibrils on the cell surface. Moreover, the N-terminal cleavage product of brevican, but not the full-length protein, associates with fibronectin in cultured cells and in surgical samples of glioma. Taken together, our results provide the first evidence of the cellular and molecular mechanisms that may underlie the motility-promoting role of brevican in primary brain tumors. In addition, these results underscore the important functional implications of brevican processing in glioma progression.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.