{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Tamborini M"],"funding":["Ministero dell'Università e della Ricerca","AIRC fellowship for Italy","FRRB grant NEVERMIND","AIRC per la Ricerca sul Cancro","Fondazione Umberto Veronesi","National Plan for Complementary Investments","Ministero dell’Università e della Ricerca","Welch Foundation"],"pagination":["2843-2860"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12908494"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["27(11)"],"pubmed_abstract":["Background
Although 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.Methods
Extracellular 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 investigate"],"journal":["Neuro-oncology"],"pubmed_title":["Extracellular vesicles released by glioblastoma cancer cells drive tumor invasiveness via Connexin-43 gap junctions."],"pmcid":["PMC12908494"],"funding_grant_id":["IG 18851","CP2_16/2018","AQ-1507","CUP B53C22006100001","PRIN2020PBS5MJ","IG 24905","22546"],"pubmed_authors":["Tamborini M","Matteoli M","Florio E","Pozzi D","Riva M","Franzone D","Sironi A","Saulle C","Fraviga E","Passoni L","Ribecco V","Pizzocri M","Lodato S","Politi LS","Pessina F","Martano G","Jiang JX","Tambalo M","Cortese K","Stanzani E","Gagliani MC","Mattioli M"],"additional_accession":[]},"is_claimable":false,"name":"Extracellular vesicles released by glioblastoma cancer cells drive tumor invasiveness via Connexin-43 gap junctions.","description":"Background
Although 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.Methods
Extracellular 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 investigate","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Nov","modification":"2026-07-15T22:15:18.556Z","creation":"2026-07-09T10:20:32.303Z"},"accession":"S-EPMC12908494","cross_references":{"pubmed":["39883079"],"doi":["10.1093/neuonc/noaf013"]}}