Antineoplastic Effects of α-Santalol on Estrogen Receptor-Positive and Estrogen Receptor-Negative Breast Cancer Cells through Cell Cycle Arrest at G2M Phase and Induction of Apoptosis.docVIP

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Antineoplastic Effects of α-Santalol on Estrogen Receptor-Positive and Estrogen Receptor-Negative Breast Cancer Cells through Cell Cycle Arrest at G2M Phase and Induction of Apoptosis.doc

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Antineoplastic Effects of α-Santalol on Estrogen Receptor-Positive and Estrogen Receptor-Negative Breast Cancer Cells through Cell Cycle Arrest at G2M Phase and Induction of Apoptosis

AntineoplasticEffectsofa-SantalolonEstrogen Receptor-PositiveandEstrogenReceptor-Negative BreastCancerCellsthroughCellCycleArrestatG2/M PhaseandInductionofApoptosis SreevidyaSantha1,AjayBommareddy2,BrittnyRule2,RuthGuillermo1,RadheySKaushik3,4, AlanYoung4,ChandradharDwivedi1* 1DepartmentofPharmaceuticalSciences,SouthDakotaStateUniversity,Brookings,SouthDakota,UnitedStatesofAmerica,2DepartmentofPharmaceuticalSciences, Wilkes University, Wilkes-Barre, Pennsylvania, United States of America, 3Department of Biology and Microbiology, South Dakota State University, Brookings, South Dakota,UnitedStatesofAmerica,4DepartmentofVeterinaryandBiomedicalSciences,SouthDakotaStateUniversity,Brookings,SouthDakota,UnitedStatesofAmerica Abstract Anticancerefficacyandthemechanismofactionofa-santalol,aterpenoidisolatedfromsandalwoodoil,wereinvestigated in human breast cancer cells by using p53 wild-type MCF-7 cells as a model for estrogen receptor(ER)-positive and p53 mutatedMDA-MB-231cellsasamodelforER-negativebreastcancer.a-Santalolinhibitedcellviabilityandproliferationin a concentration and time-dependent manner in both cells regardless of their ER and/or p53 status. However, a-santalol produced relatively less toxic effect on normal breast epithelial cell line, MCF-10A. It induced G2/M cell cycle arrest and apoptosisinbothMCF-7andMDA-MB-231cells.Cellcyclearrestinducedbya-santalolwasassociatedwithchangesinthe proteinlevelsofBRCA1,Chk1,G2/Mregulatorycyclins,Cyclindependentkinases(CDKs),Celldivisioncycle25B(Cdc25B), Cdc25CandSer-216phosphorylationofCdc25C.Anup-regulatedexpressionofCDKinhibitorp21alongwithsuppressed expressionofmutatedp53wasobservedinMDA-MB-231cellstreatedwitha-santalol.Onthecontrary,a-santaloldidnot increase the expression of wild-type p53 and p21 in MCF-7 cells. In addition, a-santalol induced extrinsic and intrinsic pathwaysofapoptosisinbothcellswithactivationofcaspase-8andcaspase-9.Itledtotheactivationoftheexecutioner caspase-6 and caspase-7 in a-santalol-treated