Aim:To investigate the apoptosis-inducing effect of cheliensisin A(GC-51),anovel styryl-lactone isolated from Goniothalamus cheliensis,on humanpromyelocytic leukemia HL-60 cells and the mechanism of action involved.Methods:Apoptotic cell death was determined by morphological examination andDNA agarose gel electrophoresis.The activity of caspase-3 was assessed usingWestern blotting and the expression of Bcl-2 and Bax genes was analyzed usingthe reverse transcription-polymerase chain reaction(RT-PCR)method.Results:GC-51 significantly inhibited the proliferation of HL-60 cells with an IC_(50)of 2.4±0.2μmol/L and effectively induced apoptosis in HL-60 cells.Exposure of HL-60cells to 10μmol/L GC-51 for 8 h resulted in approximately 53% of the cells under-going apoptosis.Caspase-3 was activated in GC-51-treated cells,which was mani-fested by the appearance of the 17 kDa active form of caspase-3 and the cleavageof poly(ADP-ribose)polymerase(PARP).Meanwhile,GC-51 markedly reducedthe expression of the anti-apoptotic gene Bcl-2 and increased the expression ofthe pro-apoptotic gene Bax.The apoptosis-inducing effect of GC-51 was cAMP-dependent protein kinase(PKA)dependent because PKA,but not the proteinkinase C,specific inhibitor H-89,blocked the induction of apoptosis by GC-51 inHL-60 cells.Conclusion:The results demonstrate that GC-51 effectively inducesapoptosis in HL-60 cells and that this effect is PKA-dependent and involves thedownregulation of Bcl-2 expression and the activation of caspase-3. Aim: To investigate the apoptosis-inducing effect of cheliensisin A (GC-51), anovel styryl-lactone isolated from Goniothalamus cheliensis, on human promyelocytic leukemia HL-60 cells and the mechanism of action involved. Methods: Apoptotic cell death was determined by morphological examination andDNA agarose gel electrophoresis.The activity of caspase-3 was assessed using Western blotting and the expression of Bcl-2 and Bax genes was analyzed using the reverse transcription-polymerase chain reaction (RT-PCR) method. Results: GC-51 significantly inhibited proliferation of HL-60 cells with an IC 50 (50) of 2.4 ± 0.2 μmol / L and effectively induced apoptosis in HL-60 cells. Expose of HL-60 cells to 10 μmol / L GC-51 for 8 h resulted in approximately 53% of the cells under-going apoptosis. Caspase-3 was activated in GC-51-treated cells, which was mani-fested by the appearance of the 17 kDa active form of caspase-3 and the cleavage of poly (ADP-ribose) polymerase ). Meanwhile, GC-51 markedly reduced the express ion of the anti-apoptotic gene Bcl-2 and increased the expression of the pro-apoptotic gene Bax. The apoptosis-inducing effect of GC-51 was cAMP-dependent protein kinase (PKA) dependent because PKA, but not the proteinkinase C, specific Inhibitor H-89, blocked the induction of apoptosis by GC-51 in HL-60 cells. Confluence: The results demonstrate that GC-51 effectively inducesapoptosis in HL-60 cells and that this effect is PKA- dependent and involves the downregulation of Bcl-2 expression and the activation of caspase-3.