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Bcl-2 overexpression prevents daunorubicin-induced apoptosis through inhibition of XIAP and Akt degradation

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Author(s)
박종욱권택규
Alternative Author(s)
Park, Jong WookKwon, Taeg Kyu
Publication Year
2003
Abstract
Daunorubicin (DNR) induces apoptosis in the human myeloid leukemia cells by activation of neutral sphingomyelinease and ceramide production. In the present study, we determined the effect of the antiapoptosis protein Bcl-2 on caspase-3 activation, phospholipase C-γ1 (PLC-γ1) degradation and cytochrome c release during the DNR-induced apoptosis. Treatment with 3 μM DNR for 12 hr produced morphological features of apoptosis and DNA fragmentation in U937 cells, which was associated with caspase-3 activation and PLC-γ1 degradation. Induction of apoptosis was also accompanied by release of cytochrome c, down-regulation of X-linked inhibitor of apoptosis protein (XIAP), and inactivation of Akt, which was blocked by the pan-caspase inhibitor z-VAD-fmk. DNR-induced caspase-3 activation, PLC-γ1 degradation and apoptosis were significantly attenuated in Bcl-2 overexpressing U937/Bcl-2 cells. Ectopic expression of Bcl-2 appeared to inhibit DNR-induced apoptosis by interfering with inhibition of XIAP and Akt degradation. Keywords
Daunorubicin;
Apoptosis;
Caspase;
XIAP;
Akt;
Bcl-2
Department
Dept. of Immunology (면역학)
Publisher
School of Medicine
Citation
Biochemical Pharmacology, Vol.66(9) : 1179-1786, 2003
Type
Article
ISSN
0006-2952
DOI
10.1016/S0006-2952(03)00545-8
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35186
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