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

Juan C Acosta, Jesús Gil

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

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 GROalpha] delays both replicative senescence and impairs the senescence response to oncogenic signals. Our findings suggest that signaling by IL-8 and GROalpha 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 GROalpha.
Original languageEnglish
Pages (from-to)2167-70
Number of pages4
JournalCancer Research
Issue number6
Publication statusPublished - 15 Mar 2009

Keywords / Materials (for Non-textual outputs)

  • Animals
  • Neoplasms
  • Cell Aging
  • Receptors, Interleukin-8B
  • Humans
  • Chemokine CXCL1
  • Interleukin-8
  • Signal Transduction


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