简介：Emodin(1,3,8-trihydroxy-6-methylanthraquinone)couldenhancethesensitivityoftumorcellstoarsenictrioxide(As2O3)-inducedapoptosisviagenerationofROS,butthemolecularmechanismhasnotbeenelucidated.Here,wecarriedoutcDNAmicroarray-basedglobaltranscriptionprofilingofHeLacellsinresponsetoAs2O3/emodincotreatment,comparingwithAs2O3-onlytreatment.Theresultsshowedthattheexpressionofanumberofgeneswassubstantiallyalteredattwotimepoints.Thesegenesareinvolvedindifferentaspectsofcellfunction.Inadditiontoredoxregulationandapoptosis,ROSaffectgenesencodingproteinsassociatedwithcellsignaling,organellefunctions,cellcycle,cytoskeleton,etc.ThesedatasuggestthatbasedonthecytotoxicityofAs2O3,emodinmobilizeeverygenomicresourcethroughwhichtheAs2O3-inducedapoptosisisfacilitated.