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KMID : 1140120080130010001
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Cancer Prevention Research
2008 Volume.13 No. 1 p.1 ~ p.11
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DNA Damage-induced Cell Death by Apoptosis
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Lee Shin-Hwa
Choi Yung-Hyun
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Abstract
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Recent data indicate that following the induction of DNA damage, a prominent route of cell inactivation is apoptosis, and specific DNA lesions that trigger apoptosis have been identified. These include O6-methylguanine, base N-alkylations, bulky DNA adducts, DNA cross-links and DNA double-strand breaks (DSBs). The complex network of regulation of DNA repair, cell-cycle checkpoints and apoptotic regulators and/or executors that determines the switch between pro- and anti-apoptotic signaling also has to be clarified. Furthermore, translation of the rapidly expanding knowledge on apoptosis that is triggered by DNA-damaging anticancer drugs into the clinic will be a real challenge for future research. Thus, strategies might be employed to enhance the apoptotic effect of genotoxic anticancer drugs by inhibiting DNA repair and anti-apoptotic functions, or by amplifying pro-apoptotic molecules. Cell death that follows DNA damage is not merely a consequence of inactivation of the genome. It is rather based on complex enzymatic reactions that might lead to apoptosis, necrosis, autophagy and other forms of cell death. This review focuses on the apoptotic response that follows the induction of DNA damage. (Cancer Prev Res 13, 1-11, 2008)
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KEYWORD
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DNA-damaging agents, Genotoxin, Repair, Methyaltion, Apoptosis
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