akt抑制剂鱼藤素对膀胱癌t24细胞生长的影响及机制的分析.docx

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1、akt抑制剂鱼藤素对膀胱癌t24细胞生长的影响及机制的分析AbstractObjective：TostudytheeffectsofAktinhibitordeguelinonthegrowthofhumanbladdercancercelllinesT-24,andtoelucidatethepossiblemechanismofsucheffects.AndToexplorewhetherinhibitionofBI3KAktsignalpathwayincreasesthetumor-killingeffectsofanticancerdrugscisplatinandPaclitaxe

2、lonbladdercancerT24cells.ThisresearchobjectiveprovideanewtheoryforAktinhibitordeguelintargetedtherapyofbladdercancerandinhibitionofBI3KAktsignalpathwayenhancethechemosensitivityofbladdercancer.Methods：MTTmethodwasusedtodeterminegrowth-inhibitoryeffectofdeguelinonhumanbladdercancerT_24cells.Apoptosis

3、inducedbydeguelininT_24cellswasdeterminedusingDNAfragmentationassay.WoundhealingtestwasusedtomeasurethemigrationabilityofT_24cells.Thecellcyclewasdetectedbyflowcytometry(1CM).TheexpressionOfMDV2andGSK3inmRN.AandproteinlevelsweredetectedbyRT-PCRandWesternblottingrespectively.TheinhibitoryrateofT_24ce

4、llsaftertreatmentwithdifferentconcentrationsofindividualdeguelin,cisplatin.Paclitaxelanddeguelinpluscisplatin.PaclitaxelwereobservedbyMTTassay,andtheircellcycleweredetectedbyflowcytometry.Results：ThecleguelinSingnificantlyinhibitedcellproliferation,blockedthecel1cycleintheGOG1phaseandinducedapoptosi

5、sinT_24cells.Themigrationcapacityofdeguelin-treatedcelIswasdecreasedcomparedwiththatofthenegativecontrolcells.TheexpressionlevelsofMDM2mRNandproteinweredown-regulated,whiletheexpressionlevelsofGSK3mRNAandproteinswereup-regulatedwhenT_24cellweretreatedbydeguelin.Theinhibitionrat100fproliferationofT24cellswasincreasedsignificantlybycisplatin,Paclitaxelincombinationwithdeguelin.deguelinhadsynergisticeffectswithcisplatin,Paclitaxel,Flowcytometryshowedthatdeguelinandcisplatin,Paclitaxelblockedthecel1cyclemainlyintheGOG1stage,whilethecombinedmedicationlengthentheGO.