Epithelial cell senescence: an adaptive response to pre-carcinogenic stresses?

被引:56
作者
Abbadie, Corinne [1 ]
Pluquet, Olivier [1 ]
Pourtier, Albin [1 ]
机构
[1] Univ Lille, Inst Pasteur Lille, CNRS, UMR Mech Tumorigenesis & Targeted Therapies M3T 8, F-59000 Lille, France
关键词
Keratinocytes; Mammary epithelial cells; SASP; DNA damage; DSB; SSB; p16; p38MAPK; p53; PARP1; Oxidative stress; Proteostasis; Unfolded protein response; Autophagy; Aging; Cancer; HUMAN ORAL KERATINOCYTES; HUMAN-PAPILLOMAVIRUS TYPE-16; ONCOGENE-INDUCED SENESCENCE; STRAND BREAK REPAIR; DNA-DAMAGE RESPONSE; SMALL BILE-DUCTS; CHAPERONE-MEDIATED AUTOPHAGY; INDUCED PREMATURE SENESCENCE; TO-MESENCHYMAL TRANSITION; PRIMARY BILIARY-CIRRHOSIS;
D O I
10.1007/s00018-017-2587-9
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Senescence is a cell state occurring in vitro and in vivo after successive replication cycles and/or upon exposition to various stressors. It is characterized by a strong cell cycle arrest associated with several molecular, metabolic and morphologic changes. The accumulation of senescent cells in tissues and organs with time plays a role in organismal aging and in several age-associated disorders and pathologies. Moreover, several therapeutic interventions are able to prematurely induce senescence. It is, therefore, tremendously important to characterize in-depth, the mechanisms by which senescence is induced, as well as the precise properties of senescent cells. For historical reasons, senescence is often studied with fibroblast models. Other cell types, however, much more relevant regarding the structure and function of vital organs and/or regarding pathologies, are regrettably often neglected. In this article, we will clarify what is known on senescence of epithelial cells and highlight what distinguishes it from, and what makes it like, replicative senescence of fibroblasts taken as a standard.
引用
收藏
页码:4471 / 4509
页数:39
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