Anti-Tumor Activity of a Novel Compound-CDF Is Mediated by Regulating miR-21, miR-200, and PTEN in Pancreatic Cancer 英文参考文献.docVIP

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Anti-Tumor Activity of a Novel Compound-CDF Is Mediated by Regulating miR-21, miR-200, and PTEN in Pancreatic Cancer 英文参考文献.doc

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Anti-Tumor Activity of a Novel Compound-CDF Is Mediated by Regulating miR-21, miR-200, and PTEN in Pancreatic Cancer 英文参考文献

Anti-TumorActivityofaNovelCompound-CDFIs MediatedbyRegulatingmiR-21,miR-200,andPTENin PancreaticCancer BinBao1.,ShadanAli2.,DejuanKong1,SanilaH.Sarkar1,ZhiweiWang1,SanjeevBanerjee1 ,Amro Aboukameel2,SubhashPadhye3,PhilipA.Philip2,FazlulH.Sarkar1* 1DepartmentofPathology,WayneStateUniversity,Detroit,Michigan,UnitedStatesofAmerica,2DivisionofHematology/OncologyKarmanosCancerInstitute,Wayne StateUniversity,Detroit,Michigan,UnitedStatesofAmerica,3Dr.D.Y.PatilUniversity,Pimpri,Pune,India Abstract Background: The existence of cancer stem cells (CSCs) or cancer stem-like cells in a tumor mass is believed to be responsiblefortumorrecurrencebecauseoftheirintrinsicandextrinsicdrug-resistancecharacteristics.Therefore,targeted killingofCSCswouldbeanewerstrategyforthepreventionoftumorrecurrenceand/ortreatmentbyovercomingdrug- resistance. We have developed a novel synthetic compound-CDF, which showed greater bioavailability in animal tissues such as pancreas, and also induced cell growth inhibition and apoptosis, which was mediated by inactivation of NF-kB, COX-2,andVEGFinpancreaticcancer(PC)cells. Methodology/PrincipalFindings:Inthecurrentstudyweshowed,forthefirsttime,thatCDFcouldsignificantlyinhibitthe sphere-formingability(pancreatospheres)ofPCcellsconsistentwithincreaseddisintegrationofpancreatospheres,which wasassociatedwithattenuationofCSCmarkers(CD44andEpCAM),especiallyingemcitabine-resistant(MIAPaCa-2)PCcells containinghighproportionofCSCsconsistentwithincreasedmiR-21anddecreasedmiR-200.Inaxenograftmousemodel ofhumanPC,CDFtreatmentsignificantlyinhibitedtumorgrowth,whichwasassociatedwithdecreasedNF-kBDNAbinding activity,COX-2,andmiR-21expression,andincreasedPTENandmiR-200expressionintumorremnants. Conclusions/Significance:Theseresultsstronglysuggestthattheanti-tumoractivityofCDFisassociatedwithinhibitionof CSCfunctionviadown-regulationofCSC-associatedsignalingpathways.Therefore,CDFcouldbeusefulfortheprevention oftumorrecurrenceand/ortreatmentofPCwithbettertreatmentoutcome