il6诱导卵巢癌细胞产生化疗耐药的作用及作用机制研究-study on the effect and mechanism of il - 6 inducing chemotherapy resistance in ovarian cancer cells.docx

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2018-05-29 发布于上海
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il6诱导卵巢癌细胞产生化疗耐药的作用及作用机制研究-study on the effect and mechanism of il - 6 inducing chemotherapy resistance in ovarian cancer cells.docx

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il6诱导卵巢癌细胞产生化疗耐药的作用及作用机制研究-study on the effect and mechanism of il - 6 inducing chemotherapy resistance in ovarian cancer cells

apoptosis-inhibitinggenesinA2780cells.Moreover,stablecelllinesoverexpressingordeletingofIL-6wereclonedtoinvestigatetheeffectofIL-6onthesensitivitytocisplatinandpaclitaxel,theexpressionlevelsofdrugresistance-associatedgenesandapoptosis-inhibitinggenes.Meanwhile,wealsoanalyzedtherelatedsignalpathwaysofchemotherapyresistancecausedbyexogenousIL-6orendogenousoverexpressingofIL-6inovariancancercellsthroughPD98059(inhibitorofMEK1/2)andWortmannin(inhibitorofPI3K).Results:Theresearchoffourcellsshow:(1)FourovariancancercellsallconstitutivelyexpressedIL-6exceptA2780.ThemRNAlevelsofIL-6resembledit’srespectiveproteinlevels.AlsofourcellsallexpressedIL-6Rαandgp130.(2)Thesensentivitytocisplatinandpaclitaxelinfourovariancancercellsisdifferent.A2780cellsarethemostsensentive,ES-2cellsareless,whereasCAOV-3andSKOV-3cellsaredrug-resistant.(3)Theexpressionlevelsofdrugresistance-associatedgenesandapoptosis-inhibitinggenesarelowerinA2780andES-2cells,wherethosearehigherinCAOV-3andSKOV-3cells.BasedontheresearchofA2780cellandSKOV3cell,wefindoutthat:(1)ExogenousIL-6cansignificantlyreducethesensitivitytocisplatinandpaclitaxelinA2780,butincreasesexpressionofdrugresistance-associatedgenesMDR1,GST-πandapoptosis-inhibitinggenesBcl-2,Bcl-xL,XIAPbyadose-dependentmanner.(2)StablyexpressionrecombinantssIL-6clonesincloudeA2780/ssIL-6L,A2780/ssIL-6M,A2780/ssIL-6H,andasIL-6clonesincludeSKOV3/asIL-6MI,SKOV3/asIL-6HIandtheirrespectiveemptyvectorwereobtained.(3)Thedrugresistancetocisplatinandpaclitaxel,expressionlevelsofdrugresistance-associatedgenesandapoptosis-inhibitinggenesinthessIL-6transfectedcellswereincreasedcomparedwiththeemptyvectorpcDNA3.1(+)/A2780clonesandnon-transfectedA2780cells,whereasthoseintheasIL-6transfectedcellsweredecreasedcomparedwiththeemptyvectorpcDNA3.1(+)/SKOV3clonesandnon-transfectedSKOV3cells.(4)PretreatmentofA2780cellswithPD98059(inhibitorofMEK1/2)andWortmannin(inhibitorofPI3K)canblockexogenousIL-6-inducedcisplatinandpaclitaxelresistance,alsotheinhibitionwasfoundinA2780/IL-6(H)clo