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

Cell Proliferation Group, Medical Research Council Clinical Sciences Centre, Faculty of Medicine, Imperial College, Hammersmith Campus, London, United Kingdom

^* To whom correspondence should be addressed. E-mail: jesus.gil{at}csc.mrc.ac.uk.

	Abstract

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] delays both replicative senescence and impairs the senescence response to oncogenic signals. Our findings suggest that signaling by IL-8 and GRO 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. [Cancer Res 2009;69(6):2167–70]

Key Words: CXCR2, IL-8, senescence