简介:Intrinsicapoptosis,apossibleresponsetomitochondrialdamage,inMDA-MB-231cellsexposedtodifferentdosesofcarbonionswasinvestigatedinthisstudy.WeassessedBaxandBcl-2expressionandcytochromecreleaseinthemitochondriaandcytosolofcellsexposedtolow(0.5Gy)andhigh(3Gy)dosesofcarbonionsusingwesternblotanalysis.
简介:近似所有人的癌症表演正常TP53基因表示的一半但是MDM2或MDMX的异常overexpression。这个事实建议有希望的癌症在指向在p53和MDM2/MDMX之间的相互作用的治疗学的策略。为了帮助,实现开发有效禁止者破坏p53-MDM2/MDMX相互作用的目标,我们系统地调查了结构并且有它和从用随机的分子的动力学模拟的一个原子论的观点的MDM2和MDMX的相互作用的禁止者的p53的相互作用特征。我们发现在MDM2和MDMX玩的结构的某特定的helices在他们的绑定给角色调音到禁止者,并且氢契约在MDM2或MDMX与它的对应物由p53的Trp23残余形成了,这在vivo从MDM2-p53建筑群决定MDM2-p53相互作用的混乱和p53的代替的动态比赛过程。结果在这报导纸被期望为设计功能的禁止者并且认识到癌症基因治疗的新策略提供基本信息。
简介:AlterationsinDNArepair,cellcycle,andapoptoticpathwaysareoftenassociatedwithcancerriskandradiationsensitivity.IndividualswithreducedDNAdamageresponsefaceagreatersensitivitytomutagenchallenge.Interindividualvariabilityinmutagenorradiationsensitivityandincancersusceptibilitymayalsobetracedbacktopolymorphismsofgenesaffectinge.g.DNArepaircapacity[1].
简介:Non-smallcelllungcancer(NSCLC)accountsfor85%oflungcancer,whichistheleadingcauseofdeathinlungcancerpatient.RoutinetreatmentofNSCLCcannoteffectivelychangethesurvivalrateofpatients,oneimportantreasonistheincreasedradioresistanceoftumorcellsafterconventionalradiotherapy.
简介:TodepictthedetailsthatCHOP(C/EBPhomologousprotein)regulatesautophagyandapoptosisinbreastcancercells,theexpressionofCHOPwasinhibitedbytransfectionwithsiRNAsequence.AsshowninFig.1,radiati-Fig.1CHOPinhibitionbysiRNAatmRNAandproteinlevelsafterradiation.onelicitedahigherexpressionofCHOPintheNCgroupcomparedwithcontrol.However,thishigherexpressionwassignificantlyinhibitedinthesiRNAgroup.