Molecular Cancer Therapeutics · 2009 · 63 citations · 26 references
MedicineOncologyPharmacologyCell SignalingMetastasisSignal TransductionCancer Cell SignalingCell MigrationMalignant NeoplasmsSignal Transduction In CancerTumor InvasionTyrosine Kinase InhibitorsCancer Cell MigrationEgfr InhibitionErk SignalingExtracellular Signal-regulated Kinase PathwayExtracellular Signal-regulated Kinase SignalingPlatelet-derived Growth Factor Receptor SignalingPlatelet-derived Growth Factor ReceptorsTyrosine Kinase Inhibitor Therapy
Platelet-derived growth factor (PDGF) receptor (PDGFR) expression correlates with metastatic medulloblastoma. PDGF stimulation of medulloblastoma cells phosphorylates extracellular signal-regulated kinase (ERK) and promotes migration. We sought to determine whether blocking PDGFR activity effectively inhibits signaling required for medulloblastoma cell migration and invasion. DAOY and D556 human medulloblastoma cells were treated with imatinib mesylate (Gleevec), a PDGFR tyrosine kinase inhibitor, or transfected with small interfering RNA (siRNA) to PDGFRB to test the effects of blocking PDGFR phosphorylation and expression, respectively. PDGFR cell signaling, migration, invasion, survival, and proliferation following PDGF-BB stimulation, with and without PDGFR inhibition, were measured. PDGF-BB treatment of cells increased PDGFRB, Akt and ERK phosphorylation, and transactivated epidermal growth factor receptor (EGFR), which correlated with enhanced migration, survival, and proliferation. Imatinib (1 μmol/L) treatment of DAOY and D556 cells inhibited PDGF-BB- and serum-mediated migration and invasion at 24 and 48 h, respectively, and concomitantly inhibited PDGF-BB activation of PDGFRB, Akt, and ERK but increased PTEN expression and activity. Imatinib treatment also induced DAOY cell apoptosis at 72 h and inhibited DAOY and D556 cell proliferation at 48 h. siRNA silencing of PDGFRB similarly inhibited signaling, migration, and survival and both siRNA and imatinib treatment inhibited PDGF-BB-mediated EGFR transactivation, indicating that the effects of imatinib treatment are specific to PDGFRB target inhibition. These results indicate that PDGFRB tyrosine kinase activity is critical for migration and invasion of medulloblastoma cells possibly by transactivating EGFR; thus, imatinib may represent an important novel therapeutic agent for the treatment of medulloblastoma.
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Paul M. Zeltzer, James M. Boyett, Jonathan L. Finlay et al. · Journal of Clinical Oncology · 1999 · 756 citations
Medicine, Oncology, Pediatrics +17
PDGF-BB induces intratumoral lymphangiogenesis and promotes lymphatic metastasis
Renhai Cao, Meit A. Björndahl, Piotr Religa et al. · Cancer Cell · 2004 · 529 citations
Medicine, Cancer Biology, Oncology +14