Cellular Senescence and the Immune System in Cancer

被引:78
|
作者
Prieto, Luis I. [1 ]
Baker, Darren J. [1 ,2 ]
机构
[1] Mayo Clin, Dept Biochem & Mol Biol, 200 1st ST SW, Rochester, MN 55905 USA
[2] Mayo Clin, Dept Pediat & Adolescent Med, Rochester, MN USA
基金
美国国家卫生研究院;
关键词
Cellular senescence; Tumorigenesis; Immunosenescence; Senolytics; CELLS; P16(INK4A); CLEARANCE; APOPTOSIS; GROWTH; TUMORIGENESIS; INHIBITION; PI3K-GAMMA; TARGET; SWITCH;
D O I
10.1159/000500683
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
In response to a variety of cancer-inducing stresses, cells may engage a stable cell cycle arrest mechanism, termed cellular senescence, to suppress the proliferation of preneoplastic cells. Despite this cell intrinsic tumor suppression, senescent cells have also been implicated as active contributors to tumorigenesis by extrinsically promoting many hallmarks of cancer, including evasion of the immune system. Here, we discuss these dual, and seemingly contradictory, roles of senescence during tumorigenesis. Furthermore, we highlight findings of how senescent cells can influence the immune system and discuss the possibility that immune cells themselves may be acquiring senescence-associated alterations. Lastly, we discuss how senescent cell avoidance or clearance may impact pathology.
引用
收藏
页码:505 / 512
页数:8
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