Development of Resistance towards Artesunate in MDA-MB-231 Human Breast Cancer Cells 英文参考文献.docVIP

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Development of Resistance towards Artesunate in MDA-MB-231 Human Breast Cancer Cells 英文参考文献.doc

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Development of Resistance towards Artesunate in MDA-MB-231 Human Breast Cancer Cells 英文参考文献

DevelopmentofResistancetowardsArtesunateinMDA- MB-231HumanBreastCancerCells BeatriceBachmeier1,2,IdunaFichtner3,PeterH.Killian1,EmanuelKronski1,UlrichPfeffer2 ,Thomas Efferth4* 1DepartmentofClinicalChemistryandClinicalBiochemistry,Ludwig-Maximilians-University,Munich,Germany,2FunctionalGenomics,AdvancedBiotechnologyCenter, Genoa, Italy, 3Department of Experimental Pharmacology, Max Delbru¨ck-Center for Molecular Medicine, Berlin, Germany, 4Department of Pharmaceutical Biology, InstituteofPharmacyandBiochemistry,JohannesGutenbergUniversity,Mainz,Germany Abstract Breast cancer is the most common cancer and the second leading cause of cancer death in industrialized countries. Systemic treatment of breast cancer is effective at the beginning of therapy. However, after a variable period of time, progression occurs due to therapy resistance. Artesunate, clinically used as anti-malarial agent, has recently revealed remarkable anti-tumor activity offering a role as novel candidate for cancer chemotherapy. We analyzed the anti-tumor effects of artesunate in metastasizing breast carcinoma in vitro and in vivo. Unlike as expected, artesunate induced resistanceinhighlymetastatichumanbreastcancercellsMDA-MB-231.Likewiseacquiredresistanceledtoabolishmentof apoptosis andcytotoxicity inpre-treated MDA-MB-231 cells. Incontrast, artesunate wasmorecytotoxic towardsthe less tumorigenic MDA-MB-468cells without showingresistance. Unraveling theunderlyingmolecular mechanisms, wefound thatresistancewasinducedduetoactivationofthetumorprogressionrelatedtranscriptionfactorsNFkBandAP-1.Thereby transcription,expressionandactivityofthematrix-degradingenzymeMMP-1,whosefunctioniscorrelatedwithincreased invasionandmetastasis,wasup-regulateduponacquisitionofresistance.Additionally,activationoftheapoptosis-related factorNFkBleadtoincreasedexpressionofant-apoptoticbcl2andreducedexpressionofpro-apoptoticbax.Applicationof artesunateinvivoinamodelofxenograftedbreastcancershowed,thattumorsgrowthwasnotef