ArticleMolecular cancer research : MCR2017
Heparan Sulfate Glycosaminoglycans in Glioblastoma Promote Tumor Invasion.
Article in Molecular cancer research : MCR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
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- Autophagy in brain tumors: molecular mechanisms, challenges, and therapeutic opportunities.Journal of translational medicine · 2025Review
- Biomarkers in glioblastoma and degenerative CNS diseases: defining new advances in clinical usefulness and therapeutic molecular target.Frontiers in molecular biosciences · 2025Article
- 6-O-endosulfatases in tumor metastasis: heparan sulfate proteoglycans modification and potential therapeutic targets.American journal of cancer research · 2024Review
- Article
- Dexamethasone Inhibits Heparan Sulfate Biosynthetic System and Decreases Heparan Sulfate Content in Orthotopic Glioblastoma Tumors in Mice.International journal of molecular sciences · 2023Article
- Review
- The multifaceted mechanisms of malignant glioblastoma progression and clinical implications.Cancer metastasis reviews · 2022Review
- In-Depth Matrisome and Glycoproteomic Analysis of Human Brain Glioblastoma Versus Control Tissue.Molecular & cellular proteomics : MCP · 2022Article
- LncRNA MALAT1 functions as a biomarker of no-reflow phenomenon in ST-segment elevation myocardial infarction patients receiving primary percutaneous coronary intervention.Scientific reports · 2022Article
- Glycomaterials to Investigate the Functional Role of Aberrant Glycosylation in Glioblastoma.Advanced healthcare materials · 2022Review
- Multiple Irradiation Affects Cellular and Extracellular Components of the Mouse Brain Tissue and Adhesion and Proliferation of Glioblastoma Cells in Experimental System In Vivo.International journal of molecular sciences · 2021Article
- Heparan Sulfate Synthesized byMolecular cancer research : MCR · 2021Article
- Chemotherapy-Induced Degradation of Glycosylated Components of the Brain Extracellular Matrix Promotes Glioblastoma Relapse Development in an Animal Model.Frontiers in oncology · 2021Article
- Endothelial cell-specific reduction of heparan sulfate suppresses glioma growth in mice.Discover oncology · 2021Article
- A Key Pathway to Cancer Resilience: The Role of Autophagy in Glioblastomas.Frontiers in oncology · 2021Review
- Prediction of Ubiquitin Ligase Nrdp1-Associated Proteins in Glioma Database.Cell biochemistry and biophysics · 2020Article
- Heparanase potentiates the invasion and migration of pancreatic cancer cells via epithelial‑to‑mesenchymal transition through the Wnt/β‑catenin pathway.Oncology reports · 2020Article
- Chemoradiotherapy Increases Intratumor Heterogeneity of HPSE Expression in the Relapsed Glioblastoma Tumors.International journal of molecular sciences · 2020Article
- Proteoglycans as Therapeutic Targets in Brain Cancer.Frontiers in oncology · 2020Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most common primary malignant brain tumor of adults and confers a poor prognosis due, in part, to diffuse invasion of tumor cells. Heparan sulfate (HS) glycosaminoglycans, present on the cell surface and in the extracellular matrix, regulate cell signaling pathways and cell-microenvironment interactions. In GBM, the expression of HS glycosaminoglycans and the enzymes that regulate their function are altered, but the actual HS content and structure are unknown. However, inhibition of HS glycosaminoglycan function is emerging as a promising therapeutic strategy for some cancers. In this study, we use liquid chromatography-mass spectrometry analysis to demonstrate differences in HS disaccharide content and structure across four patient-derived tumorsphere lines (GBM1, 5, 6, 43) and between two murine tumorsphere lines derived from murine GBM with enrichment of mesenchymal and proneural gene expression (mMES and mPN, respectively) markers. In GBM, the heterogeneous HS content and structure across patient-derived tumorsphere lines suggested diverse functions in the GBM tumor microenvironment. In GBM5 and mPN, elevated expression of sulfatase 2 (SULF2), an extracellular enzyme that alters ligand binding to HS, was associated with low trisulfated HS disaccharides, a substrate of SULF2. In contrast, other primary tumorsphere lines had elevated expression of the HS-modifying enzyme heparanase (HPSE). Using gene editing strategies to inhibit HPSE, a role for HPSE in promoting tumor cell adhesion and invasion was identified. These studies characterize the heterogeneity in HS glycosaminoglycan content and structure across GBM and reveal their role in tumor cell invasion.
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