DNA damage-dependent cell cycle checkpoints and genomic stability.
In response to genotoxic stress, which can be caused by environmental or endogenous genotoxic insults such as ionizing or ultraviolet radiation, various chemicals and reactive cellular metabolites, cell cycle checkpoints which slow down or arrest cell cycle progression can be activated, allowing the cell to repair or prevent the transmission of damaged or incompletely replicated chromosomes. Checkpoint machineries can also initiate pathways leading to apoptosis and the removal of a damaged cell from a tissue. The balance between cell cycle arrest and damage repair on one hand and the initiation of cell death, on the other hand, could determine if cellular or DNA damage is compatible with cell survival or requires cell elimination by apoptosis. Defects in these processes may lead to hypersensitivity to cellular stress, and susceptibility to DNA damage, genomic defects, and resistance to apoptosis, which characterize cancer cells. In this article, we have noted recent studies of DNA damage-dependent cell cycle checkpoints, which may be significant in preventing genomic instability.
Ishikawa
Kazuhiro
K
Jichi Medical School, Tochigi, Japan.
Ishii
Hideshi
H
Saito
Toshiyuki
T
D000818:Animals; D017209:Apoptosis / Q000235:genetics / Q000502:physiology; D002453:Cell Cycle / Q000235:genetics* / Q000502:physiology; D018797:Cell Cycle Proteins / Q000378:metabolism; D002470:Cell Survival / Q000235:genetics / Q000502:physiology; D004249:DNA Damage; D004260:DNA Repair; D018816:Genes, cdc; D042822:Genomic Instability; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
D018797:Cell Cycle Proteins