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JCI online early table of contents: March 14, 2011
Date:3/14/2011

polices cancer growth by regulating c-Jun

Cancer growth occurs due to uncontrolled cell division, which can result from the loss of proteins that repress cell cycle progression (tumor suppressors) or by increases in the amount or activity of proteins that promote cell cycle progression (oncogenes). In many cancers, loss of the tumor suppressor p53 activity is an important contributing factor to the uncontrolled cell growth. Thus, identifying the factors that contribute to controlling p53 levels has been of interest to cancer researchers. In cultured cancer cells, the protein Cop1 has been shown to target p53 for degradation, and thus there has been interest in developing inhibitors of Cop1 as cancer therapeutics.

In this paper, Jean-Christophe Marine at the Laboratory For Molecular Cancer Biology Leuven, Belgium developed a series of mouse models that demonstrate that in contrast to predictions, loss of Cop1 does not affect p53 levels or activity. Rather, Cop1 targets for degradation a protein that promotes cell cycle progression called c-Jun, and loss of Cop1 resulted in spontaneous cancer formation in the mice. The researchers believe that these findings suggest that Cop1 itself acts as a tumor suppressor, and that c-Jun, rather than p53, is its primary target in this context. In the accompanying commentary, Wenyi Wei of Beth Israel Deaconess Medical Center and William Kaelin, from Dana Farber Cancer Institute, in Boston, Massachusetts, stress that these findings suggest that inhibitors of Cop1 are unlikely to be effective cancer therapeutics, and may even enhance tumor growth.

TITLE: Cop1 constitutively regulates c-Jun protein stability and functions as a tumor suppressor in mice

AUTHOR CONTACT:
Jean-Christophe Marine
VIB-KULeuven, Leuven, BEL
Phone: 003216330368; Fax: ; E-mail: JeanChristophe.Marine@cme.vib-kuleuven.be
View this article at:

Contact: Kathryn Claiborn
press_releases@the-jci.org
Journal of Clinical Investigation
Source:Eurekalert

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