Functional cross talk between CXCR4 and PDGFR on glioblastoma cells is essential for migration.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 24023874.
- Also identified by DOI 10.1371/journal.pone.0073426 and PMC identifier 3759384.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
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.
Medical subject headings
- Chemotaxis
- Glioblastoma
- Receptor Cross-Talk
- Receptor, Platelet-Derived Growth Factor beta
- Receptors, CXCR4