Stress-Induced (Premature) Senescence

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 s-galactosidase (SA-sgal) 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-s1, p38MAPK, IGF-R1 and DNA damage. The possible induction of this type of senescence in vivo and in cancer treatment is discussed.