Expression of Eukaryotic Initiation Factor 5A and Hypusine Forming Enzymes in Glioblastoma Patient Samples Implications for New Targeted Therapies 英文参考文献.docVIP
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Expression of Eukaryotic Initiation Factor 5A and Hypusine Forming Enzymes in Glioblastoma Patient Samples Implications for New Targeted Therapies 英文参考文献
ExpressionofEukaryoticInitiationFactor5Aand
HypusineFormingEnzymesinGlioblastomaPatient
Samples:ImplicationsforNewTargetedTherapies
MichaelPreukschas1,ChristianHagel2,AlexanderSchulte3,KristofferWeber4,KatrinLamszus3,
HenningSievert1,NoraPa¨llmann1,CarstenBokemeyer1,JoachimHauber5,MelanieBraig1,
StefanBalabanov1*
1Department of Oncology, Haematology and Bone Marrow Transplantation with Section Pneumology, Hubertus Wald-Tumorzentrum, University Medical Center
Hamburg-Eppendorf, Hamburg, Germany, 2Department of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany, 3Department of
Neurosurgery,UniversityMedicalCenterHamburg-Eppendorf,Hamburg,Germany,4ResearchDepartmentCellandGeneTherapy,ClinicforStemCellTransplantation,
UniversityMedicalCenterHamburg-Eppendorf,Hamburg,Germany,5Heinrich-Pette-Institute–LeibnizInstituteforExperimentalVirology,Hamburg,Germany
Abstract
Glioblastomasarehighlyaggressivebraintumorsofadultswithpoorclinicaloutcome.Despiteabroadrangeofnewand
morespecifictreatmentstrategies,therapyofglioblastomasremainschallengingandtumorsrelapseinallcases.Recent
workdemonstratedthattheposttranslationalhypusinemodificationoftheeukaryoticinitiationfactor5A(eIF-5A)isacrucial
regulator of cell proliferation, differentiation and an important factor in tumor formation, progression and maintenance.
HerewereportthateIF-5Aaswellasthehypusine-formingenzymesdeoxyhypusinesynthase(DHS)anddeoxyhypusine
hydroxylase (DOHH) are highly overexpressed in glioblastoma patient samples. Importantly, targeting eIF-5A and its
hypusinemodificationwithGC7,aspecificDHS-inhibitor,showedastrongantiproliferativeeffectinglioblastomacelllines
invitro, while normal human astrocytes were not affected. Furthermore, we identified p53 dependent premature
senescence, a permanent cell cycle arrest, as the primary outcome in U87-MG cells after treatment with GC7. Strikingly,
combined treatment with clinically relevant alkylating agents and GC7 had an additive antiproliferative
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