A role for CXCR2 in senescence, but what about in cancer?

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 interleukm (IL)-8 or GROa] delays both replicative senescence and impairs the senescence response to oncogenic signals. Our findings suggest that signaling by IL-8 and GROa. might limit tumor growth by reinforcing senescence early in t urn or i genesis. The challenge remains in how to integrate this with the well-known tumor promoting effects of IL-8 and GROct. © 2009 American Association for Cancer Research.