Cellular Senescence: Many Roads, One Final Destination

被引:12
作者
Saab, Raya [1 ]
机构
[1] Amer Univ Beirut, Childrens Canc Ctr Lebanon, Beirut, Lebanon
来源
THESCIENTIFICWORLDJOURNAL | 2010年 / 10卷
关键词
senescence; tumor suppression; p53; Rb; DNA damage; heterochromatin; oncogene; ONCOGENE-INDUCED SENESCENCE; REACTIVE-OXYGEN; DNA-DAMAGE; PREMATURE SENESCENCE; TRIGGERS SENESCENCE; BETA-GALACTOSIDASE; INDUCE SENESCENCE; HUMAN-CELLS; IN-VITRO; TUMOR;
D O I
10.1100/tsw.2010.68
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Cellular senescence is a tumor-suppressor mechanism that has been shown to occur in response to multiple signals, including oncogenic stress, DNA damage, oxidative stress, telomere shortening, and other tumor-promoting insults. Over the past decade, much has been uncovered regarding the phenotype of this tumor-suppressor response and the underlying pathways necessary for its establishment. However, we have also learned that the intricate details of signaling pathways underlying senescence as a tumor-suppressor response are very much context dependent. In addition, cross-talk among pathways, and negative and positive feedback loops, all complicate our understanding of this process. This short review attempts to summarize what is known to date regarding senescence in tumor suppression, both in vitro and in vivo. Further insights into pathways necessary for senescence will hopefully identify appropriate targets for interventions to not only induce senescence as a treatment of cancerous lesions, but also to maintain this state in premalignant lesions in an effort to prevent progression to cancer.
引用
收藏
页码:727 / 741
页数:15
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