4.7 Review

DNA Damage Stress: Cui Prodest?

期刊

出版社

MDPI
DOI: 10.3390/ijms20051073

关键词

cell cycle checkpoints; genomic instability; G2-arrest; cell death; repair of DNA damage; adaptation

资金

  1. Associazione Italiana per la Ricerca sul Cancro, AIRC
  2. Italian Ministry of Education, University and Research-Dipartimenti di Eccellenza [L. 232/2016]
  3. Associazione Malati di Hailey-Hailey Disease, A.AMA.HHD-Onlus

向作者/读者索取更多资源

DNA is an entity shielded by mechanisms that maintain genomic stability and are essential for living cells; however, DNA is constantly subject to assaults from the environment throughout the cellular life span, making the genome susceptible to mutation and irreparable damage. Cells are prepared to mend such events through cell death as an extrema ratio to solve those threats from a multicellular perspective. However, in cells under various stress conditions, checkpoint mechanisms are activated to allow cells to have enough time to repair the damaged DNA. In yeast, entry into the cell cycle when damage is not completely repaired represents an adaptive mechanism to cope with stressful conditions. In multicellular organisms, entry into cell cycle with damaged DNA is strictly forbidden. However, in cancer development, individual cells undergo checkpoint adaptation, in which most cells die, but some survive acquiring advantageous mutations and selfishly evolve a conflictual behavior. In this review, we focus on how, in cancer development, cells rely on checkpoint adaptation to escape DNA stress and ultimately to cell death.

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