Abstract
Three main roads lead to senescence: telomere-dependent replicative senescence, oncogene-induced senescence and stress-induced (premature) senescence. This latter type of senescence appears after exposure of normal, immortalized or transformed cells to stress of chemical or physical nature inducing oxidative stress and/or DNA damage. After these exposures, chronic or acute, single or multiple, stressed cells developed a “senescence-like” phenotype. This “senescence-like” phenotype presents several biomarkers of cellular senescence such as irreversible growth arrest, morphological change, senescence-associated ß-galactosidase (SA-ßgal) activity and senescence-associated secretory phenotype (SASP). However, large-scale studies of transcriptome and proteome of cells in replicative senescence or in stress-induced senescence show that although they share similarities, the two phenotypes are not identical. Different signaling pathways involved in the development of stress-induced senescence are presented as those dependent on TGF-ß1, p38MAPK, IGF-R1 and DNA damage. The possible induction of this type of senescence in vivo and in cancer treatment is discussed.
Keywords
- Replicative senescence
- Cell cycle
- Stress
- SIPS
- Oxidation
- DNA damage
- Telomeres
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Acknowledgments
O. Toussaint, F. Debacq-Chainiaux and Marie Toutfaire are respectively Senior Research Associate, Research Associate and recipient of a Televie grant of the FNRS, Belgium. We thank the European Commission and the DG06 of the Walloon Region of Belgium for Large-scale integrating Collaborative projects “Nanovalid” (#NMP-FP7-2010-1.3-1) and “Nanoreg” (#310584), for “Qnano” (#INFRASTRUCTURE-2010-1-262163) and “Caregiver” (#1318184) projects.
The authors declare no conflict of interest.
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Debacq-Chainiaux, F., Ben Ameur, R., Bauwens, E., Dumortier, E., Toutfaire, M., Toussaint, O. (2016). Stress-Induced (Premature) Senescence. In: Rattan, S., Hayflick, L. (eds) Cellular Ageing and Replicative Senescence. Healthy Ageing and Longevity. Springer, Cham. https://doi.org/10.1007/978-3-319-26239-0_13
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