简介：ThechronicinfectionofhepatitisBvirus(HBV)iscloselyrelatedtotheoccurrenceanddevelopmentofhepatocellularcarcinoma(HCC).AccumulatedevidencehasshownthatHBVXprotein(HBxprotein)isamultifunctionalregulatorwithacrucialroleinhepatocarcinogenesis.However,informationonthemechanismbywhichHBVinducesHCCislacking.ThisreviewfocusesonthepathologicalfunctionsofHBxinHBV-inducedhepatocarcinogenesis.Asatransactivator,HBxcanmodulatenuclearfactorkappa-light-chain-enhancerofactivatedBcells(NF-κB)andtranscriptionfactorAP-2.Moreover,HBxcanaffectregulatorynon-codingRNAs(ncRNAs)includingmicroRNAsandlongncRNAs(lncRNAs),suchasmiRNA-205andhighlyupregulatedinlivercancer(HULC),respectively.HBxisalsoinvolvedinepigeneticmodification,includingmethylationandacetylation.HBxinteractswithvarioussignal-transductionpathways,suchasproteinkinaseB/Akt,Wnt/β-catenin,signaltransducerandactivatoroftranscription,andNF-κBpathways.Moreover,HBxaffectscellularfatebyshiftingthebalancetowardcellsurvival.HBxmayleadtothelossofapoptoticfunctionsordirectlycontributestooncogenesisbyachievingtransformingfunctions,whichinducehepatocarcinogenesis.Additionally,HBxcanmodulateapoptosisandimmuneresponsebydirectorindirectinteractionwithhostfactors.WeconcludethatHBxhastensthedevelopmentofhepatoma.

简介：人的间充质的干细胞(hMSCs)装家到肿瘤地点并且禁止肿瘤细胞的生长。很少对内在的分子的机制被知道连接hMSCs到肿瘤房间的指向的抑制。在这研究，我们从hMSCs用一个动物移植模型，一个合作文化系统和调节媒介在二根人的hepatoma房间线(H7402和HepG2)上调查了hMSCs的效果。当SCID老鼠与H7402细胞和Z3hMSCs的一个相等的数字被注射时，动物移植研究证明肿瘤形成的潜伏的时间被延长并且肿瘤尺寸更小。当co有教养时与Z3房间，H7402细胞增殖减少了，增加的apoptosis，和Bcl-2的表示，c-Myc，原子抗原(PCNA)和survivin低是的增殖的房间调整了。在有调节媒介的处理源于Z3hMSC文化以后，H4702房间出现了减少的形成殖民地的能力和减少的增长。Immunoblot分析证明beta-catenin，Bcl-2，c-Myc，PCNA和survivin表示是在H7402和HepG2房间调整的down。总起来说，我们的调查结果证明hMSCs禁止H7402和HepG2人的肝癌症房间线的恶意的显型，它包括增长，形成殖民地的能力和oncogene表示试管内和体内。而且，我们的研究提供表明小径的Wnt可以在调停hMSC的指向和肿瘤房间抑制有一个角色的证据。

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简介：ToclarifytheroleofAPOBEC3G(A3G)incellulardefenseagainsthepatitisBvirus(HBV),theexpressionofA3GinnormalhumanliverandtheregulationoftheA3Gexpressioninhep-atomacellline(HuH-7)wereinvestigated.ExpressionlevelofAPOBEC3smRNAinhumanliverwasdeterminedbyRT-PCR.HuH-7andHepG2cellsweretreatedwithvariousconcentrationsofIFN-α(0U/ml,100U/ml,500U/ml,1000U/ml)for12h.ThemRNAlevelsweremeasuredbyaquantitativeRT-PCR,theresultswerenormalizedrelativetothespecimenswithoutIFN-αstimulation.TotalproteinofHuH-7cellstreatedwithvariousconcentrationsofIFN-αfor48hwassubjectedtoWesternblotanalysis.Forreportergeneassay,HuH-7cellsweretransfectedwiththereporterplasmidscontainingIRF-Esitesanditsmutantswithdifferentlengths.Thenthecellsweretreatedwithorwithout1200U/mlIFN-aforadditional12h(1000U/ml)after24hoftransfection,andthecelllysatewaspreparedandassayedforluciferaseactivity.ItwasfoundthatnormalhumanliverexpressedthemRNAofA3G.A3GmRNAexpressioninHuH-7andHepG2cellswereup-regulatedbyIFN-αstimulationinadose-depen-dentmanner.WesternblotanalysisindicatedthatA3GproteinexpressionwasalsoenhancedbyIFN-αstimulation.SequenceanalysisshowedtheexistenceofputativesitesofIFNregulatoryfactorelement(IRF-E)in5'regionofA3Ggeneupstreamtheinitiationcodon.IFN-αstimulationresultsin6-to8-foldincreaseinluciferaseactivityincellstransfectedwiththeplasmidcontainingIRF-Esitesofthe5'upstreamsequences,whereasluciferaseactivitydidnotchangeincellstransfectedwiththeplasmidcontainingmutantIRF-EsitesorwithoutIRF-Esites.Asaconclusion,A3Gareexpressedinnormalhumanliver.A3Gexpressionwasup-regulatedbyIFN-αstimulationinhepatomacellsandcouldbeinvolvedinhostdefensemechanismsagainstHBV.ERF-Esitein5'regionofAP0BEC3Ggeneupstreamtheinitiationcodonplaysanimportantroleinthisp

简介：Telomeraseactivitywasinhibitedinadoseandtime-dependentmannerwiththetreatmentofcisplatinfor24,48,or72hinaconcentrationrangedfrom0.8to50μMinBEL-7404humanhepatomacells.Therewerenochangesinexpressionpatternofthreetelomerasesubunits,itscatalyticreversetranscriptasesubunit(hTERT),itsRNAcomponent(hTR)ortheassociatedproteinsubunit(TP1),aftercisplatintreatedfor72hwithindicatedconcentrations.Meantelomerelengthsweredecreasedbythecisplatintreatment.CellgrowthinhibitionandcellcycleaccumulationinG2/Mphasewerefoundtobecorrelatedwithtelomeraseinhibitioninthepresentstudy,butpercentagesofcellapoptosisdidnotchangemarkedlyduringtheprocess.

简介：Anon-radioisotopic,quantitativeTRAP-basedtelomeraseactivityassaywasestablishedmainlybyusingSYBRGreen-Istaininginsteadofradioisotope.Comparingwithconventionalradioisotopebasedmethod,itwasbetterinreproducibilityandaccuracy.Usingthismethod,wefoundtelomeraseactivitieswereabsentinnormalhumanlivercells,whiledetectedinalloffourhumanhepatomacelllines(BEL-7404,SMMC-7721,QGY-07903andHCCM)withoutsignificantdifferences.

简介：Objective:Toinvestigatetheimpactofbeta-elemeneinjectiononthegrowthandalpha-tubuleofhumanhepatocarcinomaHepG2cells.Methods:CellproliferationwasassessedbyMTTassay.Cellcycledistributionwasdetectedbyflowcytometry(FCM).ThemRNAexpressionofalpha-tubulinwasmeasuredbyRT-PCR.Westernblotanalysiswasusedtodetermineproteinexpressionofalpha-tubulinandthepolymerizationoftubulin.Results:Beta-elemeneinjectioninhibitedHepG2cellsproliferationinadose-andtime-dependentmanner;FCManalysisindicatedbeta-elemeneinjectioninducedcellcyclearrestedatSphase.RT-PCRandwesternblotanalysisshowedthatbeta-elemeneinjectiondown-regulatedalpha-tublinatbothmRNAandproteinlevels,presentingadose-dependentmanner.Moreover,beta-elemeneinjectionreducedthepolymerizationofmicrotubulesinadose-dependentmanner.Conclusions:Beta-elemeneinjectioncaninhibittheproliferationofhepatomaHepG2cellsandinducecellapoptosis,themechanismmightbepartlyrelatedtothedown-regulationofalpha-tubulinandinhibitionofmicrotubularpolymerization.

简介：瞄准：学习三氧化二砷的anti-hepatoma效率(作为(2)O(3))在试验性的老鼠肝细胞的治疗，癌(HCC)由2-acetamidofluorene(2-FAA)导致了并且阐明可能的机制。方法：SD老鼠(2瞬间旧)用2-FAA被喂了让8wk导致HCC，然后他们被对待与作为(2)O(3)或妈三倍。在d上29，老鼠被打死，肝被称，肝肿瘤被数。肝织物的组织学的变化在显微镜下面被观察，并且细胞的动态参数被流动血细胞计数学习。Immunohistochemistry(二拍子的圆舞方法)被用来在连续的节上观察脉管的内皮生长因素(VEGF)和微容器的密度(MVD)的表示。病理学的参数也被分析，浆液aspartateaminotransferase(著名计算机生产厂商)的层次，丙氨酸aminotransferase(中高音)，全部的胆红素(TBi)，和直接胆红素(DBi)。结果：肝肿瘤的数字在对待与的组显著地减少了作为(2)O(3)，在特别中等剂量(1mg/kg)组织(t=2.80，P<0.01)。当(2)O(3)经由apoptosis引起了HCC细胞死亡；坏死被看见，当剂量是1mg/kg时，apoptosis是普通的。增长索引严厉地减少了在中等剂量(1mg/kg)组织(7.87+/-4.11对24.46+/-6.49，t=2087，P<0.01)，然而并非在0.2mg/kg组。然而，S阶段部分在两个组戏剧性地减少了，仅仅当剂量与控制相比是1mg/kg时，它到达了底部水平(0.40+/-0.13对3.01+/-0.51，t=2.97，P<0.01)，并且它显然在G(0)/G(1)(G(0)/G(1)限制)伴有房间的累积。VEGF和MVD在的表情中等剂量(1mg/kg)组比生理盐水组显著地低(0.63+/-0.74对2.44+/-0.88，P<0.05；15.75+/-3.99对47.44+/-13.41，t=2.80，P<0.01)。与生理盐水组相比，是的中等剂量、低剂量的组(2)O(3)和妈三倍在浆液降低了中高音的层次(61.46+/-9.46，63.75+/-20.40，61.18+/-13.00对108.98+/-29.86，t=2.14，P<0.05)，但是没有浆液著名计算机生产厂商诚实

简介：AIM:Toinvestigatetheanti-apoptoticcapabilityofthehepatitisBvirus(HBV)intheHepG2hepatomacelllineandtheunderlyingmechanisms.METHODS:CellviabilityandapoptosisweremeasuredbyMTTassayandflowcytometry,respectively.Targetedknockdownofmanganesesuperoxidedismutase(MnSOD),AMP-activatedproteinkinase(AMPK)andhepatitisBvirusXprotein(HBx)genesaswellasAMPKagonistAICARandantagonistcompoundCwereemployedtodeterminethecorrelationsofexpressionofthesegenes.RESULTS:HBVmarkedlyprotectedthehepatomacellsfromgrowthsuppressionandcelldeathintheconditionofserumdeprivation.AdecreaseofsuperoxideanionproductionaccompaniedwithanincreaseofMnSODexpressionandactivitywasfoundinHepG2.215cells.Moreover,AMPKactivationcontributedtotheup-regulationofMnSOD.HBxproteinwasidentifiedtoinducetheexpressionofAMPKandMnSOD.CONCLUSION:OurresultssuggestthatHBVsuppressesmitochondrialsuperoxidelevelandexertsanantiapoptoticeffectbyactivatingAMPK/MnSODsignalingpathway,whichmayprovideanovelpharmacologicalstrategytopreventHCC.

简介：AIM:Toinvestigatetheantitumoractivityofadriamycin(ADR)encapsulatedinnanoparticles(NADR)andinjectedintothehepaticarteryofhepatoma-bearingrats.METHODS:NADRwaspreparedbytheinterfacialpolymerizationmethod.Walker-256carcinosarcomasweresurgicallyimplantedintotheleftliverlobesof60maleWistarrats,whichweredividedinto4groupsatrandom(15ratspergroup).Onthe7thdayafterimplantation,normalsaline(NS),freeADR(FADR),NADR,orADRmixedwithunloadednanoparticles(ADR+NP)wasrespectivelyinjectedviathehepaticartery(i.a.)ofratsindifferentgroups.ThedoseofADRineachformulationwas2.0mg/kgbodyweightandtheconcentrationwas1.0mg/mL.Survivaltime,tumorenlargementratio,andtumornecrosisdegreewerecomparedbetweeneachgroup.RESULTS:ComparedwiththeratsthatreceivedNSi.a.,theratsthatreceivedFADRorADR+NPacquiredapparentinhibitionontumorgrowth,aswellasprolongedtheirlifespan.Furthersignificantanticancerefficacywasobservedinratsthatreceivedi.a.administrationofNADR.StatisticsindicatedthatNADRbroughtonamoresignificanttumorinhibitionandmoreextensivetumornecrosis,ascomparedtoFADRorADR+NP.Themeantumorenlargementratioonthe7thdayafterNADRi.a.was1.106.Themeantumorbearingsurvivaltimewas39.50days.Prolongedlifespanratiowas109.22%ascomparedwithratsthatacceptedNS.CONCLUSION:TherapeuticeffectofADRonlivermalignancycanbesignificantlyenhancedbyitsnanopaticleformulationandadministrationviahepaticartery.

简介：Havingbeenpassedfor160generations,acelllinedesignatedasH22-F25/LwasestablishedfromamurinetumorlymphaticmetastatlcmodelH22-F25whichhadbeensetupinourcollege.Thecelllinewasinsuspensionculturewitharapidproliferationandstablegrowth.Thepeaktuneofcelldivisionandproliferationwas48and96hoursafterculture.Inaweek,thecellnumberwasIncreasedby25tunes.H22-F25/Lstillkeepsthefeaturesofapoorlydifferentiatedcancer.Itstumorinducingrate(invivo)was100%in615mice.Lymphnodemetastasisratewas50%andpulmonarymetastasisrate10%.H22-F25/LIsapopulationofheterogenetlctumorcellsIncluding2stemcelllines(themodelnumberofchromosomesbeing43in40%tumorcellsand86in32%)andsomesidelines.ThecommonmarkerchromosomesM1,M2,M3andM4werepresentinallstemandsidelines.

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