Anti-Angiogenic Therapy Induces Integrin-Linked Kinase 1 Up-Regulation in a Mouse Model of Glioblastoma 英文参考文献.docVIP

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Anti-Angiogenic Therapy Induces Integrin-Linked Kinase 1 Up-Regulation in a Mouse Model of Glioblastoma 英文参考文献.doc

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Anti-Angiogenic Therapy Induces Integrin-Linked Kinase 1 Up-Regulation in a Mouse Model of Glioblastoma 英文参考文献

Anti-AngiogenicTherapyInducesIntegrin-LinkedKinase 1Up-RegulationinaMouseModelofGlioblastoma ChiaraVerpelli1,2,4,GiulioBertani1,4,ValentinaCea1,2,MonicaPatti1,2,AndreasBikfalvi1,3 ,Lorenzo Bello1,4*,CarloSala1,2 * 1ELAT (European Laboratory for Angiogenesis and Translational Research), University of Milan, Milan, Italy, 2CNR Neuroscience Institute and Department of Pharmacology,UniversityofMilan,Milan,Italy,3INSERMU920(exE0113)andUniversityofBordeaux1,Talence,France,4Neurosurgery,DepartmentofNeurological Sciences,UniversityofMilan,Milan,Italy Abstract Background: In order to improve our understanding of the molecular pathways that mediate tumor proliferation and angiogenesis,andtoevaluatethebiologicalresponsetoanti-angiogenictherapy,weanalyzedthechangesintheprotein profileofglioblastomainresponsetotreatmentwithrecombinanthumanPlateletFactor4-DLRmutatedprotein(PF4-DLR), aninhibitorofangiogenesis. Methodology/PrincipalFindings:U87-derivedexperimentalglioblastomasweregrowninthebrainofxenograftednude mice,treatedwithPF4-DLR,andprocessedforproteomicanalysis.Morethanfiftyproteinsweredifferentiallyexpressedin responsetoPF4-DLRtreatment.Amongthem,integrin-linkedkinase1(ILK1)signalingpathwaywasfirstdown-regulated butthenup-regulatedaftertreatmentforprolongedperiod.TheactivityofPF4-DLRcanbeincreasedbysimultaneously 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 correlatedtoapoorprognosis. 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 angiogenesisinhibitorsbyassociationwithspecificagentsthatdisruptsignal