Cellular senescence: a double-edged sword in the fight against cancer

被引:47
作者
Ohtani, Naoko [2 ]
Takahashi, Akiko
Mann, David J. [3 ]
Hara, Eiji [1 ]
机构
[1] Japanese Fdn Canc Res, Inst Canc, Div Canc Biol, Koto Ku, Tokyo 170, Japan
[2] Japan Sci & Technol Agcy, PRESTO, Tokyo, Japan
[3] Univ London Imperial Coll Sci Technol & Med, Div Mol Biosci, London, England
关键词
ageing; cancer; cellular senescence; NF-KAPPA-B; DNA-DAMAGE RESPONSE; TUMOR-SUPPRESSOR; LYSINE METHYLATION; IN-VIVO; REPLICATIVE SENESCENCE; SECRETORY PHENOTYPE; G(1) CONTROL; P53; P16(INK4A);
D O I
10.1111/j.1600-0625.2012.01493.x
中图分类号
R75 [皮肤病学与性病学];
学科分类号
100206 ;
摘要
Over the last few decades, it has become apparent that oncogenic proliferative signals are coupled to a variety of growth inhibitory responses, such as the induction of apoptotic cell death or irreversible cell cycle arrest known as cellular senescence. Thus, both apoptosis and cellular senescence are thought to act as important tumor suppression mechanisms. Unlike apoptotic cells, however, senescent cells remain viable for long periods of time and accumulate with increasing age in various organs and tissues. Moreover, recent studies reveal that although cellular senescence initially functions as a tumor suppressive process, it may eventually exhibit tumor-promoting effects. Therefore, it is conceivable that accumulation of senescent cells during the ageing process in vivo may contribute to the age-related increase in cancer incidence. In this review, we provide an update and perspective on recent advances made in understanding the deleterious side effects of cellular senescence.
引用
收藏
页码:1 / 4
页数:4
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