Anti-angiogenic therapy induces integrin-linked kinase 1 up-regulation in a mouse model of glioblastoma. (Articolo in rivista)

Type
Label
  • Anti-angiogenic therapy induces integrin-linked kinase 1 up-regulation in a mouse model of glioblastoma. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Alternative label
  • Verpelli C, Bertani G, Cea V, Patti M, Bikfalvi A, Bello L and Sala C (2010)
    Anti-angiogenic therapy induces integrin-linked kinase 1 up-regulation in a mouse model of glioblastoma.
    in PloS one
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Verpelli C, Bertani G, Cea V, Patti M, Bikfalvi A, Bello L and Sala C (literal)
Pagina inizio
  • e13710 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 5 (literal)
Rivista
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1 ELAT (European Laboratory for Angiogenesis and Translational Research), University of Milan, Milan, Italy, 2 CNR Neuroscience Institute and Department of Pharmacology, University of Milan, Milan, Italy, 3 INSERM U920 (ex E0113) and University of Bordeaux 1, Talence, France, 4 Neurosurgery, Department of Neurological Sciences, University of Milan, Milan, Italy (literal)
Titolo
  • Anti-angiogenic therapy induces integrin-linked kinase 1 up-regulation in a mouse model of glioblastoma. (literal)
Abstract
  • Background: In order to improve our understanding of the molecular pathways that mediate tumor proliferation and angiogenesis, and to evaluate the biological response to anti-angiogenic therapy, we analyzed the changes in the protein profile of glioblastoma in response to treatment with recombinant human Platelet Factor 4-DLR mutated protein (PF4-DLR), an inhibitor of angiogenesis. Methodology/Principal Findings: U87-derived experimental glioblastomas were grown in the brain of xenografted nude mice, treated with PF4-DLR, and processed for proteomic analysis. More than fifty proteins were differentially expressed in response to PF4-DLR treatment. Among them, integrin-linked kinase 1 (ILK1) signaling pathway was first down-regulated but then up-regulated after treatment for prolonged period. The activity of PF4-DLR can be increased by simultaneously treating mice orthotopically implanted with glioblastomas, with ILK1-specific siRNA. As ILK1 is related to malignant progression and a poor prognosis in various types of tumors, we measured ILK1 expression in human glioblatomas, astrocytomas and oligodendrogliomas, and found that it varied widely; however, a high level of ILK1 expression was correlated to a poor prognosis. Conclusions/Significance: Our results suggest that identifying the molecular pathways induced by anti-angiogenic therapies may help the development of combinaatorial treatment strategies that increase the therapeutic efficacy of angiogenesis inhibitors by association with specific agents that disrupt signaling in tumor cells. (literal)
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