A Role for CXCR2 in Senescence, but What about in Cancer?

被引:66
作者
Acosta, Juan C. [1 ]
Gil, Jesus [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, MRC, Ctr Clin Sci, Fac Med,Cell Proliferat Grp, London W12 0NN, England
关键词
CELLULAR SENESCENCE; REPLICATIVE SENESCENCE; TUMOR-GROWTH; TUMORIGENESIS; FIBROBLASTS; SECRETION; TARGET; P53;
D O I
10.1158/0008-5472.CAN-08-3772
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Senescence is an irreversible arrest triggered by stresses such as telomere shortening, DNA damage, or oncogenic signaling. Oncogene-induced senescence occurs in preneoplastic lesions, but it is absent from full-blown malignancies suggesting a tumor suppressor function. We recently found that depletion of the receptor CXCR2 [which binds to chemokines such as interleukin (IL)-8 or GRO alpha] delays both replicative senescence and impairs the senescence response to oncogenic signals. Our findings suggest that signaling by IL-8 and GRO alpha might limit tumor growth by reinforcing senescence early in tumorigenesis. The challenge remains in how to integrate this with the well-known tumor promoting effects of IL-8 and GRO alpha. [Cancer lies 2009;69(6):2167-70]
引用
收藏
页码:2167 / 2170
页数:4
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