Aim:To explore the anticancer effects and the molecular mechanisms of gambogic acid (GA) on Jurkat cells.Methods:Cell viability was assessed by 3-(4,5-dimethylthiazol-2-y1)-2,5-diphenyltetrazolium bromide assay.Annexin V-fluores-cein-isothiocyanate/propidium iodide,DNA defragmentation,and comet assay were used to detect apoptosis.Weste blotting was used to study the expres-sion of death inducer-obliterator-1 (DIO-1),Bcl-2,NF-kB,and pro-caspase 3,as well as 2 activated subunits:p17 and p20.The subcellular localization of DIO-1 was examined by immunofluorescence and Hoechst33258 staining.Results:GA inhibited the proliferation of Jurkat cells with 50% inhibitory concentration values of 1.51 ±0.09 (24 h),0.98±0.13 (48 h),and 0.67±0.12 μmol/L (72 h).GA was able to induce apoptosis of Jurkat cells.Treated by GA,the expression of DIO-1 was upregulated,and that of Bcl-2 and NF-KB was downegulated,leading to the activation ofpro-caspase 3.GA induced the translocation of DIO-1 to the nucleus.Conclusion:GA suppressed the proliferation of Jurkat cells by apoptosis induction.DIO-1 triggered early-stage cell death in GA-treated Jurkat cells.