Geranylgeranylacetone Induces Apoptosis in HL-60 Cells.

  • Okada Shohei
    Department of Cell Chemistry, Institute of Molecular and Cell Biology, Okayama University Medical School, Okayama 700-8558, Japan
  • Yabuki Munehisa
    Institute of Medical Science, Kurashiki Medical Center, Kurashiki 710-8522, Japan
  • Kanno Tomoko
    Institute of Medical Science, Kurashiki Medical Center, Kurashiki 710-8522, Japan
  • Hamazaki Keisuke
    Institute of Medical Science, Kurashiki Medical Center, Kurashiki 710-8522, Japan
  • Yoshioka Tamotsu
    Institute of Medical Science, Kurashiki Medical Center, Kurashiki 710-8522, Japan
  • Yasuda Tatsuji
    Department of Cell Chemistry, Institute of Molecular and Cell Biology, Okayama University Medical School, Okayama 700-8558, Japan
  • A. Horton Alan
    School of Biochemistry, University of Birmingham, Edgebaston, Birmingham B15 2TT, United Kingdom
  • Utsumi Kozo
    Institute of Medical Science, Kurashiki Medical Center, Kurashiki 710-8522, Japan

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抄録

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 Ras, 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.

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