"A tumor cell lacks the ability to limit its own growth," says Michele Pagano, M.D., Associate Professor of Pathology, who led the new study published in the March 11 issue of Nature. "APC puts the brake on cell growth."
The study sheds light on the relationship between APC and two other proteins involved in the development of cancer -- Skp2 and p27. APC controls the abundance of Skp2, according to the study. Skp2 determines whether a cell will begin the process of making copies of itself, and it was previously tied to p27.
"This is a very important and exciting study," says Avram Hershko, M.D., Ph.D., Distinguished Professor at Technion-Israel Institute of Technology in Haifa, who has made seminal contributions to understanding protein degradation and the cell cycle, the sequence of events a cell undergoes to make a copy of itself by dividing into two.
"Only recently has it been realized that Skp2 is a very important oncogene," Dr. Hershko explained in an e-mail. "Dr. Pagano's new study reveals how Skp2 itself is eliminated. This knowledge may be used in the future to down-regulate (decrease the activity of) Skp2 in cancers, and thus to arrest the growth of these cancers."
The gene encoding the p27 protein is one of about twenty so-called "tumors suppressor genes" that have been linked to cancer. When these genes aren't fully activated or are mutated, cells lose their ability to limit their own growth. In previous studies, low levels of the p27 protein have been associated with the development of certain tumors of the breast, colon, lung, esophagus, bone marrow, and thymus. In a sense, APC indir
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Contact: Pamela McDonnell
Pamela.McDonnell@med.nyu.edu
212-404-5555
New York University Medical Center and School of Medicine
10-Mar-2004