Geranylgeranylacetone induces apoptosis in HL-60 cells

被引：20
作者：
Okada, S
Yabuki, M
Kanno, T
Hamazaki, K
Yoshioka, T
Yasuda, T
Horton, AA
Utsumi, K
机构：
[1] Kurashiki Med Ctr, Inst Med Sci, Kurashiki, Okayama 7108522, Japan
[2] Okayama Univ, Sch Med, Inst Mol & Cell Biol, Dept Cell Chem, Okayama 7008558, Japan
[3] Univ Birmingham, Sch Biochem, Birmingham B15 2TT, W Midlands, England
来源：
CELL STRUCTURE AND FUNCTION | 1999年 / 24卷 / 03期
关键词：
geranylgeranylacetone; isoprenoid; apoptosis; HL-60; cell; caspase; isoprenylation; nitric oxide;
D O I：
10.1247/csf.24.161
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
Geranylgeranylacetone (GGA) induces apoptosis in human leukemia HL-60 cells in a dose- and time-dependent manner. This effect was completely prevented by the pan-caspase inhibitor z-Val-Ala-Asp(OMe) fluoromethylketone, thereby implicating the caspase cascade in the process. Prior to DNA fragmentation, GGA treatment markedly activated caspase-3(-like) proteases, which might be responsible for the observed apoptosis. In addition, GGA treatment interfered with the processing and membrane localization of Rap1 and Pas, and these changes may be a result of apoptosis. Moreover, nitric oxide donors significantly accentuated the GGA-induced apoptosis, suggesting that the apoptotic pathway induced by GGA might be regulated by a redox-sensitive mechanism. Taken together, these data suggest that the isoprenoid, GGA, is an effective inducer of apoptotic cell death in HL-60 cells.
引用
收藏
页码：161 / 168
页数：8
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