Next Article in Journal
Prevention or Amelioration of Autism-Like Symptoms in Animal Models: Will it Bring Us Closer to Treating Human ASD?
Next Article in Special Issue
Special Issue on DNA Replication Stress: Summary of Topics Covered
Previous Article in Journal
Gene Selection and Evolutionary Modeling Affect Phylogenomic Inference of Neuropterida Based on Transcriptome Data
Previous Article in Special Issue
Stress Marks on the Genome: Use or Lose?
Open AccessReview

DNA Damage Stress: Cui Prodest?

Department of Molecular Medicine, Sapienza University of Rome, 00161 Rome, Italy
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2019, 20(5), 1073; https://doi.org/10.3390/ijms20051073
Received: 18 January 2019 / Revised: 18 February 2019 / Accepted: 26 February 2019 / Published: 1 March 2019
(This article belongs to the Special Issue DNA Replication Stress)
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. View Full-Text
Keywords: cell cycle checkpoints; genomic instability; G2-arrest; cell death; repair of DNA damage; adaptation cell cycle checkpoints; genomic instability; G2-arrest; cell death; repair of DNA damage; adaptation
Show Figures

Graphical abstract

MDPI and ACS Style

Verma, N.; Franchitto, M.; Zonfrilli, A.; Cialfi, S.; Palermo, R.; Talora, C. DNA Damage Stress: Cui Prodest? Int. J. Mol. Sci. 2019, 20, 1073. https://doi.org/10.3390/ijms20051073

AMA Style

Verma N, Franchitto M, Zonfrilli A, Cialfi S, Palermo R, Talora C. DNA Damage Stress: Cui Prodest? International Journal of Molecular Sciences. 2019; 20(5):1073. https://doi.org/10.3390/ijms20051073

Chicago/Turabian Style

Verma, Nagendra; Franchitto, Matteo; Zonfrilli, Azzurra; Cialfi, Samantha; Palermo, Rocco; Talora, Claudio. 2019. "DNA Damage Stress: Cui Prodest?" Int. J. Mol. Sci. 20, no. 5: 1073. https://doi.org/10.3390/ijms20051073

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop