Cellular senescence: putting the paradoxes in perspective

被引:264
作者
Campisi, Judith [1 ,2 ]
机构
[1] Buck Inst Age Res, Novato, CA 94945 USA
[2] Univ Calif Berkeley, Lawrence Berkeley Lab, Berkeley, CA 94720 USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
STEM-CELLS; CANCER; SUPPRESSION; FIBROSIS; TARGET; GROWTH; TUMORS; P53;
D O I
10.1016/j.gde.2010.10.005
中图分类号
Q2 [细胞生物学];
学科分类号
071013 [干细胞生物学];
摘要
Cellular senescence arrests the proliferation of potential cancer cells, and so is a potent tumor suppressive mechanism, akin to apoptosis. Or is it? Why did cells evolve an anti-cancer mechanism that arrests, rather than kills, would-be tumor cells? Recent discoveries that senescent cells secrete growth factors, proteases and cytokines provide a shifting view from senescence as a cell autonomous suppressor of tumorigenesis to senescence as a means to mobilize the systemic and local tissue milieu for repair. In some instances, this mobilization benefits the organism, but in others it can be detrimental. These discoveries provide potential mechanisms by which cellular senescence might contribute to the diverse, and seemingly incongruent, processes of tumor suppression, tumor promotion, tissue repair, and aging.
引用
收藏
页码:107 / 112
页数:6
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