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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)
Young-Ho KimHo Cheol ShinDal Won SongSung-Hee LeeTamotsu FurumaiJong-Wook ParkTaeg Kyu Kwon
Keimyung Author(s)
Park, Jong WookKwon, Taeg KyuSong, Dal Won
Department
Dept. of Immunology (면역학)
Dept. of Otorhinolaryngology (이비인후과학)
Journal Title
Biochemical and Biophysical Research Communications
Issued Date
2003
Volume
309
Issue
2
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
Keimyung Author(s)(Kor)
박종욱
권택규
송달원
Publisher
School of Medicine
Citation
Young-Ho Kim et al. (2003). Arisostatins A induces apoptosis through the activation of caspase-3 and reactive oxygen species generation in AMC-HN-4 cells. Biochemical and Biophysical Research Communications, 309(2), 449–456. doi: 10.1016/j.bbrc.2003.07.009
Type
Article
ISSN
1090-2104
DOI
10.1016/j.bbrc.2003.07.009
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/34835
Appears in Collections:
1. School of Medicine (의과대학) > Dept. of Immunology (면역학)
1. School of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학)
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