Journal
NATURE COMMUNICATIONS
Volume 13, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-022-33235-7
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Funding
- Canadian Institutes for Health Research [CIHR FDN143322]
- Fondation Charles Bruneau (FCB)
- Canadian Foundation for Innovation [CFI10]
- Cancer Research Society (CRS)/Genome Quebec (GC)
- McGill Interdisciplinary Initiative in Infection and Immunity (MI4) program
- Jack Cole Chair in Pediatric Hematology/Oncology from the Whitehead-Penney Endowment
- Fonds de recherche du Quebec-Sante (FRQS)
- RIMUHC Desjardins Studentship in Child Health
- McGill Faculty of Medicine internal postdoctoral award
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The study reveals that extracellular vesicles from endothelial cells can promote the transition of GSCs from proneural to mesenchymal by activating MMPs and NFkB, and inactivating NOTCH.
Glioblastoma (GBM) is an incurable form of primary astrocytic brain tumor driven by glioma stem cell (GSC) compartment closely associated with the vascular niche. GSC phenotypes are heterogeneous and range from proneural to mesenchymal-like, the latter characterised by greater invasiveness. Here we document the secretory (angiocrine) role of endothelial cells and their derived extracellular vesicles (EVs) as drivers of proneural-to-mesenchymal reprogramming of GSCs. These changes involve activation of matrix metalloproteinases (MMPs) and NF kappa B, and inactivation of NOTCH, while altering responsiveness to chemotherapy and driving infiltrative growth in the brain. Our findings suggest that EV-mediated angiocrine interactions impact the nature of cellular stemness in GBM with implications for disease biology and therapy. Glioma stem-like cells (GSCs) exhibit plasticity during proneural-to-mesenchymal transition. Here the authors show that extracellular vesicles from endothelial cells can promote this transition of GSCs through activation of MMPs and NFkB, and inactivation of NOTCH.
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