Context-dependent effects of cellular senescence in cancer development

被引:144
作者
Lecot, Pacome [1 ]
Alimirah, Fatouma [1 ]
Desprez, Pierre-Yves [1 ,2 ]
Campisi, Judith [1 ,3 ]
Wiley, Christopher [1 ]
机构
[1] Buck Inst Res Aging, 8001 Redwood Blvd, Novato, CA 94945 USA
[2] Calif Pacific Med Ctr, 475 Brannan St, San Francisco, CA 94107 USA
[3] Univ Calif Berkeley, Lawrence Berkeley Natl Lab, 1 Cyclotron Rd, Berkeley, CA 94720 USA
关键词
immunosurveillance; inflammation; oncogene; senescence-associated secretory phenotype; tumour progression; tumour suppression; TUMOR SUPPRESSION; MITOCHONDRIAL DYSFUNCTION; SECRETORY PHENOTYPE; DAMAGE RESPONSE; CELLS; P53; RESTORATION; CLEARANCE; REGULATOR; APOPTOSIS;
D O I
10.1038/bjc.2016.115
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Cellular senescence is an established tumour-suppressive mechanism that prevents the proliferation of premalignant cells. However, several lines of evidence show that senescent cells, which often persist in vivo, can also promote tumour progression in addition to other age-related pathologies via the senescence-associated secretory phenotype (SASP). Moreover, new insights suggest the SASP can facilitate tissue repair. Here, we review the beneficial and detrimental roles of senescent cells, highlighting conditions under which the senescence response does and does not promote pathology, particularly cancer. By better understanding the context-dependent effects of cellular senescence, it may be feasible to limit its detrimental properties while preserving its beneficial effects, and develop novel therapeutic strategies to prevent or treat cancer and possibly other age-associated diseases.
引用
收藏
页码:1180 / 1184
页数:5
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