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Norrin对胃癌细胞凋亡的抑制作用及可能机制 Title:InhibitionofGastricCancerCellApoptosisbyNorrin:PossibleMechanisms Abstract: Gastriccancerisaleadingcauseofcancer-relateddeathsworldwide.Thedevelopmentofeffectivetherapeuticstrategiesforgastriccanceristhereforeofutmostimportance.Norrin,aproteinknownforitsroleinvasculardevelopmentandangiogenesis,hasrecentlybeenfoundtoplayaroleincancerprogression.ThisstudyaimstoinvestigatetheinhibitoryeffectofNorrinongastriccancercellapoptosisandelucidatetheunderlyingmechanisms. Introduction: Gastriccancerisacomplexandheterogeneousdiseasecharacterizedbyuncontrolledcellgrowth,invasion,andmetastasis.Dysregulationofcellapoptosis,theprogrammedcelldeathmechanism,isfrequentlyobservedincancercells,includinggastriccancer.Severalstudieshaveindicatedthatinducingapoptosisincancercellsisapromisingstrategyforcancertreatment.Norrin,asecretedglycoprotein,wasoriginallyidentifiedforitsroleinoculardevelopmentinhumans.However,recentstudieshaverevealeditsinvolvementincancerprogressionandcellsurvival. MaterialsandMethods: ToinvestigatetheeffectofNorrinongastriccancercellapoptosis,weutilizedgastriccancercelllinesandperformedvariousassays,includingcellviability,apoptosis,andmolecularanalysis.Thegastriccancercelllines(e.g.,AGS,MKN-45,andNCI-N87)weretreatedwithrecombinantNorrinprotein.CellviabilitywasassessedusingtheMTTassay,andapoptosiswasevaluatedbyAnnexinV/propidiumiodidestainingandflowcytometricanalysis.ProteinexpressionwasexaminedbyWesternblotanalysis. Results: OurresultsdemonstratedthattreatmentwithNorrineffectivelyinhibitedgastriccancercellapoptosis.TheMTTassayrevealedasignificantreductionincellviabilityfollowingNorrintreatmentcomparedtocontrolcells.AnnexinV/propidiumiodidestainingandflowcytometricanalysisconfirmedthatNorrintreatmentpromotedthesurvivalofgastriccancercellsbyinhibitingapoptosis.Furthermore,WesternblotanalysisrevealedthatNorrintreatmentsuppressedtheactivationofapoptoticmarkers,includingcaspasesandBax,whilepromotingtheanti-apoptoticmarkerBcl-2. Mechanisms: Toun