ArticleNeuro-oncology2025
Extracellular vesicles released by glioblastoma cancer cells drive tumor invasiveness via Connexin-43 gap junctions.
Article in Neuro-oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Mitochondria and exosome intercellular co-transfer via annular gap junction vesicles in the human glioblastoma stem cell niche.Human cell · 2026Article
- Extracellular Vesicles in Diffuse Midline Glioma: Emerging Mediators of Radiation Response and Therapeutic Resistance.Cancers · 2026Review
- Small and medium/large glioblastoma extracellular vesicles differentially regulate endothelial and mitochondrial function in blood-brain barrier and peripheral vasculature models.Journal of neuro-oncology · 2026Article
- Small and Large Extracellular Vesicles in Circulation of Diffuse Large B-Cell Lymphoma Patients Originate From Different Cell Types of the Tumor Microenvironment.Journal of extracellular vesicles · 2026Article
- Extracellular vesicle biomarkers: current status and future perspectives as novel tools in liquid biopsy.Frontiers in immunology · 2026Review
- Organoids glimpse: the nexus for diverse tumor heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Engineered Extracellular Vesicles in Glioma Therapy: Recent Advances and Applications.International journal of nanomedicine · 2026Review
- Connexin hemichannel blockade by abEC1.1 disrupts glioblastoma progression, suppresses invasiveness, and reduces hyperexcitability in preclinical models.Cell communication and signaling : CCS · 2025Article
- Review
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Authors and funding
22 authors.
Funding
Abstract
backgroundAlthough invasiveness is one of the major determinants of the poor glioblastoma (GBM) outcome, the mechanisms of GBM invasion are only partially understood. Among the intrinsic and environmental processes promoting cell-to-cell interaction processes, eventually driving GBM invasion, we focused on the pro-invasive role played by extracellular vesicles (EVs), a heterogeneous group of cell-released membranous structures containing various bioactive cargoes, which can be transferred from donor to recipient cells.
methodsExtracellular vesicles isolated from patient-derived GBM cell lines and surgical aspirates were assessed for their pro-migratory competence by spheroid migration assays, calcium imaging, and PYK2/FAK phosphorylation. Brain invasiveness was investigated in human cortical organoids-based assembloids and in vivo orthotopic xenografts. Extracellular vesicles' molecular features were specified by multiplex bead-based flow cytometry.
resultsResults unveil a self-sustaining mechanism triggering migration through autocrine release and engagement of a specific population of EVs of large size (L-EVs), isolated from either patient-derived cell lines or surgical aspirates. Large size-EVs act through modulation of calcium transients via Connexin 43-Gap Junctions (Cx43-GJ) and phospho-activation of PYK2. Preincubation with blocking antibodies targeting Cx43 hemichannels demonstrated a dose-dependent inhibition of the L-EV-mediated GBM migration. By exploiting patients' surgical aspirates, we show that only L-EVs deriving from tumoral cells, and not those with immune origin, promote tumor migration, impacting more prominently the tumoral cells with mesenchymal subtype.
conclusionsWe demonstrate that L-EVs released by GBM cells, but not by the immune cells of the tumor microenvironment, represent a relevant and unique autocrine pro-migratory input for the tumor.
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Registered trials
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 Socratic graph.