Skip to Main content Skip to Navigation
New interface
Journal articles

Functional cross talk between CXCR4 and PDGFR on glioblastoma cells is essential for migration.

Abstract : Glioblastoma (GBM) is the most common and aggressive form of brain tumor, characterized by high migratory behavior and infiltration in brain parenchyma which render classic therapeutic approach ineffective. The migratory behaviour of GBM cells could be conditioned by a number of tissue- and glioma-derived cytokines and growth factors. Although the pro-migratory action of CXCL12 on GBM cells in vitro and in vivo is recognized, the molecular mechanisms involved are not clearly identified. In fact the signaling pathways involved in the pro-migratory action of CXCL12 may differ in individual glioblastoma and integrate with those resulting from abnormal expression and activation of growth factor receptors. In this study we investigated whether some of the receptor tyrosine kinases commonly expressed in GBM cells could cooperate with CXCL12/CXCR4 in their migratory behavior. Our results show a functional cross-talk between CXCR4 and PDGFR which appears to be essential for GBM chemotaxis.
Document type :
Journal articles
Complete list of metadata

Cited literature [37 references]  Display  Hide  Download
Contributor : Istituto Pasteur Fondazione Cenci Bolognetti Connect in order to contact the contributor
Submitted on : Saturday, August 2, 2014 - 12:46:02 PM
Last modification on : Wednesday, November 30, 2022 - 4:14:07 PM
Long-term archiving on: : Tuesday, April 11, 2017 - 6:44:28 PM


 Restricted access
To satisfy the distribution rights of the publisher, the document is embargoed until : jamais

Please log in to resquest access to the document




Miriam Sciaccaluga, Giuseppina d'Alessandro, Francesca Pagani, Giuseppina Ferrara, Nadia Lopez, et al.. Functional cross talk between CXCR4 and PDGFR on glioblastoma cells is essential for migration.. PLoS ONE, 2013, 8 (9), pp.e73426. ⟨10.1371/journal.pone.0073426⟩. ⟨pasteur-01053840⟩



Record views