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Arisostatins A induces apoptosis through the activation of caspase-3 and reactive oxygen species generation in AMC-HN-4 cells

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Author(s)
박종욱권택규송달원
Alternative Author(s)
Park, Jong WookKwon, Taeg KyuSong, Dal Won
Publication Year
2003
Abstract
A microbial secondary metabolite, arisostatins A (As-A), was originally discovered as a substance carrying the antibiotic activity
against Gram-positive bacteria and shown to possess potent anti-tumor properties. The mechanism by which arisostatins A initiates
apoptosis remains poorly understood. In the present report we investigated the effect of arisostatins A on activation of the apoptotic
pathway in HN-4 cells. Arisostatins A was shown to be responsible for the inhibition of HN-4 cell growth by inducing apoptosis.
Treatment with 4 lM arisostatins A for 24 h produced morphological features of apoptosis and DNA fragmentation in HN-4 cells.
Arisostatins A caused dose-dependent apoptosis and DNA fragmentation of HN-4 cells used as a model. Treatment with caspase
inhibitor significantly reduced the arisostatins A-induced caspase 3 activation. In addition, arisostatins A-induced apoptosis was
associated with the generation of reactive oxygen species (ROS), which was prevented by an antioxidant NAC (N-acetyl-cysteine).
These data indicate that cytotoxic effect of arisostatins A on HN-4 cells is attributable to the induced apoptosis and that arisostatins
A-induced apoptosis is mediated by caspase-3 activation pathway, loss of mitochondrial transmembrane potential (DWm), and
release of cytochrome c into cytosol.
2003 Elsevier Inc. All rights reserved.
Keywords: Arisostatins A; Apoptosis; AMC-HN-4; ROS; Caspase 3
Department
Dept. of Immunology (면역학)
Dept. of Otorhinolaryngology (이비인후과학)
Publisher
School of Medicine
Citation
Biochemical and Biophysical Research Communications, Vol.309(2) : 449-456, 2003
Type
Article
ISSN
1090-2104
DOI
10.1016/j.bbrc.2003.07.009
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/34835
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