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没食子酸对非小细胞肺癌A549细胞增殖与凋亡的影响及机制研究.docx

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没食子酸对非小细胞肺癌A549细胞增殖与凋亡的影响及机制研究 Title:TheEffectsandMechanismsofEllagicAcidonProliferationandApoptosisinA549Non-SmallCellLungCancerCells Abstract: Non-smallcelllungcancer(NSCLC)isaleadingcauseofcancer-relatedmortalityworldwide.Despiteextensiveresearch,thedevelopmentofeffectivetreatmentsforNSCLCremainsachallenge.Ellagicacid(EA),anaturalphenoliccompoundfoundinvariousfruitsandvegetables,hasbeenreportedtopossessanticancerpropertiesagainstvarioustypesofcancers.However,theeffectsandunderlyingmechanismsofEAonNSCLCcellsremainlargelyunexplored. Inthisstudy,weaimedtoinvestigatetheimpactofEAontheproliferationandapoptosisofA549NSCLCcells.OurresultsdemonstratedthatEAsuppressedtheproliferationofA549cellsinadose-dependentmanner,asdeterminedbyMTTassay.Additionally,EAinducedcellcyclearrestattheG2/Mphase,asevidencedbyflowcytometryanalysis.Furthermore,weobservedthatEAtreatmentsignificantlypromotedapoptosisinA549cells,asindicatedbyAnnexinV-FITC/PIstainingandcaspase-3activityassay. Toelucidatetheunderlyingmechanismsinvolvedintheantiproliferativeandpro-apoptoticeffectsofEA,weexaminedtheexpressionlevelsofapoptosis-relatedproteins.WesternblotanalysisrevealedthatEAtreatmentupregulatedtheexpressionofBax,apro-apoptoticprotein,anddownregulatedtheexpressionofBcl-2,ananti-apoptoticprotein,indicatingtheinvolvementofthemitochondrialapoptosispathway.Moreover,EAtreatmentactivatedthecaspase-9/-3cascade,furthersupportingtheinvolvementofthemitochondrialpathwayinEA-inducedapoptosis. Inadditiontoitsapoptoticeffects,EAalsoexerteditsantiproliferativeactionsthroughtheinhibitionofkeysignalingpathwaysimplicatedincancerprogression.WesternblotanalysisshowedthatEAtreatmentdecreasedthephosphorylationofAktandERK1/2,twoimportantregulatorsofcellsurvivalandproliferation.ThissuggeststhatEAmaymodulatecellgrowthbyattenuatingtheAktandERK1/2signalingpathwaysinA549cells. Takentogether,ourfindingsdemonstratethatEAinhibitsproliferationandinducesapoptosisinA549NSCLCcells.Themechanismsunderlyingtheseeffectsinvolvethemodulationof