摘要
AIM:Tostudythepossibleactionsandmechanismsofperoxisomeproliferator-activatedreceptorγ(PPARγ),aligand-activatedtranscriptionfactor,inpancreaticcarcinogenesis,especiallyinangiogenesis.METHODS:ExpressionsofPPARγandretinoidacidreceptor(RXRα)wereexaminedbyreverse-transcriptionpolymerasechainreaction(RT-PCR)withimmunocytochemicalstaining.Pancreaticcarcinomacells,PANC-1,weretreatedeitherwith9-cis-RA,aligandofRXRα,orwith15-deoxy-Δ12,14prostaglandinJ2(15d-PGJ2),aligandofPPARγ,orboth.Antiproliferativeeffectwasevaluatedbycellviabilityusingmethyltetrazolium(MTT)assay.ApancreaticcarcinomaxenografttumormodelofnudemicewasestablishedbyinoculatingPANC-1cellssubcutaneously.Rosiglitazone,aspecificligandofPPARγ,wasadministeredviawaterdrinkinginexperimentalgroupofnudemice.After75d,allmiceweresacrificed.Expressionofproliferatingcellnuclearantigen(PCNA)intumortissuewasexaminedwithimmunohistochemicalstaining.Expressionofvascularendothelialgrowthfactor(VEGF)mRNAinPANC-1cells,whichweretreatedwith15d-PGJ2or9-cis-RAatvariousconcentrationsordifferentduration,wasdetectedbysemi-quantitativeRT-PCR.EffectsofRosiglitazoneonchangesofmicrovasculardensity(MVD)andVEGFexpressionwereinvestigatedinxenografttumortissue.Neovasculaturewasdetectedwithimmunohistochemistrystaininglabeledwithanti-Ⅳcollagenantibody,andindicatedbyMVD.RESULTS:RT-PCRandimmunocytochemicalstainingshowedthatPPARγandRXRαwereexpressedinPANC-1cellsatbothtranscriptionlevelandtranslationlevel.MTTassaydemonstratedthat15d-PGJ2,9-cis-RAandtheircombinationinhibitedthegrowthofPANC-1cellsinadose-dependentmanner.9-cis-RAhadacombinedinhibitingactionwith15d-PGJ2onthegrowthofpancreaticcarcinoma.InvivostudiesrevealedthatRosiglitazonesignificantlysuppressedthegrowthofpancreaticcarcinomaascomparedtocontrolgroup(0.48±0.23cm3vs2.488±0.59cm3,P<0.05),andthegro
出版日期
2009年04月14日（中国期刊网平台首次上网日期，不代表论文的发表时间）
