Arisostatins A induces apoptosis through the activation of caspase-3 and reactive oxygen species generation in AMC-HN-4 cells
- 박종욱; 권택규; 송달원
- Alternative Author(s)
- Park, Jong Wook; Kwon, Taeg Kyu; Song, Dal Won
- Publication Year
- 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
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