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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2002.1
- 수록면
- 308 - 315 (8page)
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Purpose: Arsenic trioxide (As2O3) was introduced into
the treatment of refractory or relapsed acute promyelocytic
leukemia and showed a striking effectiveness
in China and United States multicenter study. However,
the mechanistic basis for the carcinogenic or therapeutic
effects of arsenics is still poorly understood. So, this
study is performed to determine whether As2O3 induces
apoptosis through intrinsic caspase cascades in acute
promyelocytic leukemia HL-60 cells.
Materials and Methods: HL-60 cells were treated with
As2O3 to investigate apoptosis through signaling of
caspase cascades and mitochondrial dysfunction.
Results: As2O3 (>0.5 uM) decreased the viability of
HL-60 cells in a dose-dependent manner, which was
revealed as apoptosis shown chromatin condensation and
ladder pattern DNA fragmentation. As2O3 increased the
catalytic activity of caspase family cysteine proteases
including caspase-3 and -9 proteases. Consistently,
PARP, an intracellular biosubstrate of caspase-3 protease,
was cleaved from 116 kDa to 85 kDa fragments. It also
induced the change of mitochondrial membrane potential.
Morever, As2O3 resulted in the increase of Bak.
Conclusion: These data suggest that As2O3 induces
apoptosis of HL-60 cells through activation of intrinsic
caspase protease with mitochondrial dysfunction.
(Cancer Res Treat. 2002;34:308-315)
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