《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》由会员分享，可在线阅读，更多相关《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（2页珍藏版）》请在第壹文秘上搜索。
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.
