Aim:To investigate the anticancer effects and molecular mechanism of artonin Bon the human acute lymphoblastic leukemia CCRF-CEM cells compared with otherprenylflavonoid compounds.Methods:The effects of four prenylflavonoids onthe growth of CCRF-CEM and HaCa cells were studied by 3-(4,5)-2,5-diphenyl-tetrazolium bromide(MTT)assay.Apoptosis were detected through Hoechst33258 staining.The effect of artonin B on the cell cycle of CCRF-CEM cells werestudied by propidium iodide method.The change in mitochondrial membranepotential was detected by rohdamine 123 staining.The cytochrome c release andcaspase 3 activity were checked by immunoassay kits,respectively.The expres-sion of Bcl-2 family proteins was detected by Western blot.Results:Our datarevealed that artonin B strongly induced human CCRF-CEM leukemia cell death ina dose-and time-dependent manner by MTT assay,but not on normal epitheliacells(HaCa cells).Artonin B-induced cell death was considered to be apoptoticby observing the typical apoptotic morphological change by Hoechst 33258staining.The induction of human CCRF-CEM leukemia cancer cell death wascaused by an induction of apoptosis through mitochondrial membrane potentialchange,cytochrome c release,sub-G1 proportion increase,downregulation ofBcl-2 expression,upregulation of Bax and Bak expression and activation of caspase3 pathways.Conclusion:These results clearly demonstrated that artonin B isable to inhibit proliferation by induction of hypoploid cells and cell apoptosis.Moreover,the anticancer effects of artonin B were related to mitochondrial path-way and caspase 3 activation in human CCRF-CEM leukemia cells. Aim: To investigate the anticancer effects and molecular mechanism of artonin Bon the human acute lymphoblastic leukemia CCRF-CEM cells compared with other prenylflavonoid compounds. Methods: The effects of four prenylflavonoids on the growth of CCRF-CEM and HaCa cells were studied by 3- (4 , 5) -2,5-diphenyl-tetrazolium bromide (MTT) assay. Apoptosis were detected through Hoechst 33258 staining. The effect of artonin B on the cell cycle of CCRF-CEM cells were studied by propidium iodide method. Change in mitochondrial membrane potential was was detected by rohdamine 123 staining the cytochrome c release and caspase 3 activity were checked by immunoassay kits, respectively. The expres-sion of Bcl-2 family proteins was detected by Western blot. Results: Our datarevealed that artonin B strongly induced human CCRF-CEM leukemia cell death ina dose-and time-dependent manner by MTT assay, but not on normal epithelia cells (HaCa cells). Artonin B-induced cell death was considered to be apoptoticby observing the typica l apoptotic morphological change by Hoechst 33258 staging. The induction of human CCRF-CEM leukemia cancer cell death was cultured by an induction of apoptosis through mitochondrial membrane potentialchange, cytochrome c release, sub-G1 proportion increase, downregulation of Bcl-2 expression, upregulation of Bax and Bak expression and activation of caspase 3 pathways. Contact: These results show that that artonin B is able to inhibit proliferation by induction of hypoploid cells and cell apoptosis. More over, the anticancer effects of artonin B were related to mitochondrial path-way and caspase 3 activation in human CCRF-CEM leukemia cells.