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Scripps Research study reveals new function of protein kinase pathway in tumor suppression

ind out whether PRAK was essential for ras-induced senescence in vivo, and whether deletion of the PRAK gene would make a difference in the ras-induced tumor-development process in PRAK knockout mice. A group of these mice and a group of normal mice were treated with DMBA, an environmental pollutant found in cigarette smoke and gas emissions, which can induce ras mutations and cause skin tumor formation. The researchers monitored the incidence of skin tumor formation in these mice, and after tumors formed, the degree of cell senescence in the tumors. The results, Sun said, were exciting.

"The mice lacking the PRAK gene were more susceptible to skin tumor induction by DMBA, as compared to wild-type mice," Sun said. "This indicates that the presence of the normal PRAK gene suppresses tumor formation. In the wild-type, normal mice, DMBA induced premature senescence, but in the knockout tumors there were no senescent cells. The PRAK knockout animals were resistant to ras-induced senescence but prone to tumor induction, which led us to the happy conclusion that PRAK and the senescence response mediated by PRAK has a tumor-suppressing function in vivo. The knockout mice were more vulnerable to tumor induction because the senescence pathway, which is responsible for the anti-tumor self-defense mechanism, had been compromised. In addition to the skin cancer model, loss of the PRAK gene in mice also accelerates lymphoma development, which indicates that PRAK may be involved in suppressing tumor formation in multiple tissues."


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Contact: Keith McKeown
kmckeown@scripps.edu
858-784-8134
Scripps Research Institute
25-Jan-2007


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