Very interesting article in the March issue of Cancer Research Journal:
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 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.
A role for CXCR2 in senescence, but what about in cancer?
Acosta JC, Gil J.
Cancer Res. 2009 Mar 15;69(6):2167-70. Epub 2009 Mar 10.
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4 comments:
This is a very interesting article. I hope the cancer research will find cure to cancer as soon as possible.
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We recently found that depletion of the receptor carlmontpharmacy.com CXCR2 [which binds to chemokines such as interleukin (IL)-8 or GROalpha] delays both replicative senescence and impairs the senescence response to oncogenic signals.
Senescence-related genes play an important role in the process of tumor suppression, while the disruption of senescence-essential genes predisposes organisms to develop cancer. A previous animal study demonstrated that mice develop cancer at an early age due to the inactivation of p53 or p16 proteins. seattle hot water heater replacement
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