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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Induction of leukemia cell apoptosis by cheliensisin A involves down-regulation of Bcl-2 expression.

AIM: To investigate the apoptosis-inducing effect of cheliensisin A (GC-51), a novel 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 and DNA 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 the proliferation of HL-60 cells with an IC50 of 2.4+/-0.2 micromol/L and effectively induced apoptosis in HL-60 cells. Exposure of HL-60 cells to 10 micromol/L GC-51 for 8 h resulted in approximately 53% of the cells undergoing apoptosis. Caspase-3 was activated in GC-51-treated cells, which was manifested by the appearance of the 17 kDa active form of caspase-3 and the cleavage of poly(ADP-ribose) polymerase (PARP). Meanwhile, GC-51 markedly reduced the expression 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 protein kinase C, specific inhibitor H-89, blocked the induction of apoptosis by GC-51 in HL-60 cells. CONCLUSION: The results demonstrate that GC-51 effectively induces apoptosis 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.[1]

References

  1. Induction of leukemia cell apoptosis by cheliensisin A involves down-regulation of Bcl-2 expression. Zhong, L., Li, C.M., Hao, X.J., Lou, L.G. Acta Pharmacol. Sin. (2005) [Pubmed]
 
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