The prognosis of children with high-grade glioma or high-risk neuroblastoma 
remains poor. Cilengitide is a selective antagonist of αvβ3 and αvβ5 integrins, 
which are involved in tumor growth and development of metastasis. We have 
evaluated the effects of cilengitide on pediatric glioma and neuroblastoma cell 
lines for the first time. Expression levels of αvβ3 and αvβ5 were determined by 
flow cytometry in three neuroblastoma and five pediatric glioma cell lines 
compared with adult U87-MG before and after irradiation. Cell detachment, 
cytotoxicity, and cell growth under nonadhesive conditions were measured using 
the MTS assay. Cell death and apoptosis were assessed by annexin-V/propidium 
iodide staining. The varying αvβ3 and αvβ5 expression levels were unrelated to 
tumor grade. Irrespective of the αvβ5 expression level, the pediatric cells 
expressing αvβ3 were dose dependently sensitive to cilengitide. UW479 cells 
expressed only αvβ5 integrin and were not sensitive to cilengitide, suggesting 
that cilengitide's action largely depends on αvβ3 inhibition. Cell detachment 
resulted in a higher cytotoxicity in pediatric glioma compared with U87-MG 
cells, which seem able to grow despite the significant cilengitide-induced cell 
detachment. Growth kinetics on polyHEMA showed that only pediatric glioma cells 
were sensitive to anoikis and so died after cilengitide-induced detachment. 
Furthermore, irradiation of glioma cells increased αvβ3 expression slightly but 
not cilengitide sensitivity. Cilengitide's action on glioma and neuroblastoma 
cells appears to be dependent on αvβ3 expression and sensitivity to anoikis. 
Cilengitide is able to target pediatric glioma and neuroblastoma cells in vitro 
directly and efficiently. Tumor context could validate these promising 
observations.