简介：Apoptosisplaysanimportantroleinembryonicdevelopment,tissueremodeling,immuneregulationandtumorregression.Twogroupsofmolecules(Bcl-2familyand“Deathfactor”family)areinvolvedinregulatingapoptosis.InordertoknowabouttheeffectofBcl-2onapoptosisinducedbyFas,atypicalmemberof“Deathfactor”family,thetransfectionexperimentswithexpressionvectorspcDNA3-flandpcDNA3-bcl-2wereperformedinBEL-7404cells,ahumanhepatocellularcarcinomacelllinewhichexpressesendogenousFas,butnotFasLandBcl-2.ThedatashowedthattheexpressionofFasLinpcDNA3-fltransfectedhepatomacellsobviouslyinducedtheapoptosisofthecells.However,theoverexpressionofBcl-2inpcDNA3-bcl-2transfected7404/b-16cellscounteractedpcDNA3-fltransienttransfectionmediatedapoptosis.FurtherstudybycotransfectionexperimentsindicatedthatBidbutnotBax(bothwerepro-apoptoticproteinsofBcl-2family)blockedtheinhibitoryeffectofBcl-2onFas-mediatedapoptosis.TheseresultssuggestedthatFas-mediatedapoptosisinhumanhepatomacellsispossiblyregulatedbyBcl-2familyproteinsviamitochondriapathway.