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TETRASPANIN CD9: FROM NEURAL STEM CELLS TO GLIOBLASTOMA MICROENVIRONMENT CONTROL
Elvira Mª Carbonelland 5 co-authors
Universitat Jaume I
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS06-09PM-016
Presentation
Date TBA
Board: PS06-09PM-016
Event Information
Poster Board
PS06-09PM-016
Poster
View posterAbstract
Glioblastoma (GB) contains a population of glioma stem‑like cells (GSCs) that resemble adult neural stem cells (NSCs) and contribute to treatment resistance and tumour relapse. CD9 (Tspan29) is a tetraspanin enriched in NSCs in the ventricular–subventricular zone and striatum, and it is also increased in GB, where higher levels associate with invasion, resistance to cell death and worse prognosis.
In this project, we study the role of CD9 in maintaining a stem‑like state and in regulating communication between glioma cells and their microenvironment using a murine GB stem‑like cell model. We use genetic and cellular approaches to analyse how changes in CD9 affect cell proliferation, stemness and differentiation markers, both at baseline and after chemotherapy.
By combining these results with published data on CD9 in NSCs and GB, we aim to understand whether CD9 support tumour growth.
This work may help explain how a normal brain stem cell marker is reused by GB stem‑like cells and point to new ways to interfere with tumour–microenvironment communication to improve treatment response.
In this project, we study the role of CD9 in maintaining a stem‑like state and in regulating communication between glioma cells and their microenvironment using a murine GB stem‑like cell model. We use genetic and cellular approaches to analyse how changes in CD9 affect cell proliferation, stemness and differentiation markers, both at baseline and after chemotherapy.
By combining these results with published data on CD9 in NSCs and GB, we aim to understand whether CD9 support tumour growth.
This work may help explain how a normal brain stem cell marker is reused by GB stem‑like cells and point to new ways to interfere with tumour–microenvironment communication to improve treatment response.
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