Home > Browse Issues > Vol.35 No.2
DNA Damage: A Double-edge Sword in Tumor and Cellular Senescence
Li Xiaoman, Xu Hongde, Lin Meina, Song Xiaoyu, Feng Yanling, Yi Fei, Liu Shuang, Cao Liu*
Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang 110001, China
Abstract: Both exogenous and endogenous insults can result in DNA damage， which can be readily sensed
by DNA repair machinery， and consequently trigger a series of cellular events， namely “DNA Damage Response”
(DDR)， to achieve cell cycle arrest. Transient cell cycle arrest will allow DNA repair and prevent the passing of
aberrant DNA to the daughter cells. However， persistent DNA damage could result in irreversible cell proliferation
arrest (senescence) to terminate cell function， or programmed cell death (apoptosis) to eliminate impaired cells.Under circumstances of excessive accumulation of incompletely or inaccurately repaired DNA and hence gathering
of oncogenic mutations， cells may acquire unrestrictedly proliferative properties and propagate into cancer. Despite
the fact that cancer and senescence are oppositely characterized by hyperproliferation and hypoproliferation，
respectively， they are not mutually exclusive and actually driven by a unified mechanism: DNA damage.
by DNA repair machinery， and consequently trigger a series of cellular events， namely “DNA Damage Response”
(DDR)， to achieve cell cycle arrest. Transient cell cycle arrest will allow DNA repair and prevent the passing of
aberrant DNA to the daughter cells. However， persistent DNA damage could result in irreversible cell proliferation
arrest (senescence) to terminate cell function， or programmed cell death (apoptosis) to eliminate impaired cells.Under circumstances of excessive accumulation of incompletely or inaccurately repaired DNA and hence gathering
of oncogenic mutations， cells may acquire unrestrictedly proliferative properties and propagate into cancer. Despite
the fact that cancer and senescence are oppositely characterized by hyperproliferation and hypoproliferation，
respectively， they are not mutually exclusive and actually driven by a unified mechanism: DNA damage.
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