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Molecular Circuit Breaker Can Prevent Runaway Cell Growth

signals that stimulate cells to proliferate. When the strength of these signals rises to dangerous levels, ARF relays this information to another growth inhibitory protein, p53, that in turn prevents the over-stimulated cells from growing and can even induce them to commit suicide. One protein whose levels are carefully monitored by this ARF-p53 "fail-safe" mechanism is Myc, a protein that is required for normal cell growth but whose unregulated overexpression can lead to cancer.

"The ARF protein controls a p53-dependent process that helps to safeguard cells against runaway growth promoting signals," Sherr says. "ARF and p53 act together to limit Myc's stimulatory potential, but in cases where ARF is damaged and can no longer function, unchecked Myc activity can cause havoc."

Sherr and Roussel collaborated with Scott W. Lowe and his colleagues at Cold Spring Harbor Laboratory, and Carol Prives at Columbia University in an attempt to further generalize these findings. The Cold Spring Harbor researchers have been studying another tumor-inducing viral gene, called E1A. They had previously found that p53 suppresses the tumor-generating activity of E1A. The new findings reveal that this ability of cells to resist E1A also depends strongly upon ARF.

Understanding how ARF works has helped to interpret the actions of what Robert Weinberg [of the Whitehead Institute for Biomedical Research at MIT] calls 'collaborating oncogenes.' This theory posits that truly normal cells resist certain oncogenes and refuse to be transformed into cancer cells.

"We have known for 15 years that genes like Myc and E1A help to overcome this resistance. Myc and E1A kill normal cells by activating the ARF-p53 checkpoint," says Sherr, "but they also select for the emergence of rare tumor cells that have lost the ARF-p53 checkpoint and no longer die." The studies on ARF's ability to counteract the effects of Myc and E1A were published in two article
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Contact: Jim Keeley
keeleyj@hhmi.org
301-215-8858
Howard Hughes Medical Institute
7-Aug-1998


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