Sensitization of Human Pancreatic Cancer Cells Harboring Mutated K-ras to Apoptosis 英文参考文献.docVIP

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Sensitization of Human Pancreatic Cancer Cells Harboring Mutated K-ras to Apoptosis 英文参考文献.doc

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Sensitization of Human Pancreatic Cancer Cells Harboring Mutated K-ras to Apoptosis 英文参考文献

SensitizationofHumanPancreaticCancerCells HarboringMutatedK-rastoApoptosis LingShen1,Sung-HoonKim2,ChangYanChen1* 1Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts, United States of America, 2Lab of AngiogenesisandChemoprevention,GraduateSchoolofEast-WestMedicalScience,KyungheeUniversity,Seoul,SouthKorea Abstract PancreaticcancerisadevastatinghumanmalignancyandgainoffunctionalmutationsinK-rasoncogeneisobservedin 75%–90%ofthepatients.Studieshaveshownthatoncogenicrasisnotonlyabletopromotecellgrowthorsurvival,but alsoapoptosis,dependinguponcircumstances.UsingpancreaticcancercelllineswithorwithoutexpressingmutatedK-ras, wedemonstratedthattheinhibitionofendogenousPKCactivitysensitizedhumanpancreaticcancercells(MIAandPANC-1) expressing mutated K-ras to apoptosis, which had no apoptotic effect on BxPC-3 pancreatic cancer cells that contain anormalRasaswellashumanlungepithelialBAES-2Bcells.Inthisapoptoticprocess,thelevelofROSwasincreasedand PUMAwasupregulatedinap73-dependentfashioninMIAandPANC-1cells.Subsequently,caspase-3wascleaved.Afull induction of apoptosis required the activation of both ROS- and p73-mediated pathways. The data suggest that PKC is acrucialfactorthatcopeswithaberrantK-rastomaintainthehomeostasisofthepancreaticcancercellsharboringmutated K-ras.However,thesuppressionorlossofPKCdisruptsthebalanceandinitiatesanapoptoticcrisis,inwhichROSandp73 appearthepotential,keytargets. Citation: Shen L, Kim S-H, Chen CY (2012) Sensitization of Human Pancreatic Cancer Cells Harboring Mutated K-ras to Apoptosis. PLoS ONE 7(7): e40435. doi:10.1371/journal.pone.0040435 Editor:FazlulH.Sarkar,WayneStateUniversitySchoolofMedicine,UnitedStatesofAmerica ReceivedMarch20,2012;AcceptedJune6,2012;PublishedJuly25,2012 Copyright: ? 2012 Shen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse,distribution,andreproductioninanyme