CHAPEL HILL, N.C. -- New research done on insects in North Carolina and on human cells elsewhere has identified a key signaling mechanism required for normal embryonic development. When inappropriately activated, studies show, the mechanism turns healthy cells first into abnormal ones and then often into tumors.
"Our work, together with that of our colleagues, reveals for the first time the precise role of a key regulatory protein found in both insects and ourselves," said Dr. Mark Peifer, assistant professor of biology at the University of North Carolina at Chapel Hill. "We have found that this protein, called 'armadillo' in insects and 'beta-catenin' in humans, goes into the cell nucleus and helps regulate gene expression or, in other words, turns genes on and off."
In normal embryonic development, by switching genes on and off, the protein tells cells which tissues they should make and directs, for example, development of arms and legs, Peifer said. The
process occasionally goes awry, however, when beta-catenin becomes active in places where it should not. It then triggers cells to reproduce indefinitely, or it prevents them from dying, leading to benign tumors that can later become malignant.
"It is now clear that this sort of mistake underlies essentially all cases of colon cancer and many melanomas, a form of skin cancer difficult to treat," he said.
A report on the findings, supported by the National Institute of General Medical Sciences, appears in the March 21 issue of the journal Cell. Besides Peifer, UNC-CH authors are doctoral students Robert Cavallo and Joseph Loureiro. Other authors include Drs. Marc van de Wetering and Hans Clevers of University Hospital in Utrecht, Netherlands, and others at the National Cancer Institute and American and Northwestern universities.
Peifer, a member of the UNC Lineberger Comprehensive Cancer Center, also has a
commentary in Friday's (March 21) issue of
Contact: David Williamson
University of North Carolina at Chapel Hill