IRCCS Humanitas Research Hospital & Humanitas University
Published May 11, 2026 | Version v1
Dataset Open

Dataset related to article "Extracellular vesicles released by glioblastoma cancer cells drive tumor invasiveness via Connexin-43 gap junctions"

Authors/Creators

  • 1. ROR icon IRCCS Humanitas Research Hospital
  • 2. Institut Curie
  • 3. CNR Institute of Neuroscience
  • 4. ROR icon Humanitas University
  • 5. ROR icon University of Genoa
  • 6. ROR icon The University of Texas Health Science Center at San Antonio

Description

This record contains raw data related to article” Extracellular vesicles released by glioblastoma cancer cells drive tumor invasiveness via Connexin-43 gap junctions”

 

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 investigated in human cortical organoids-based assembloids and in vivo orthotopic xenografts. Extracellular vesicles’ molecular features were specified by multiplex bead-based flow cytometry.

Results

Results 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.

Conclusions

We 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.

Files

bioluminescence in vivo.zip

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Additional details

Related works

Is supplement to
Publication: 10.1093/neuonc/noaf013 (DOI)