In the study, the cover story in the Feb. 17 issue of Molecular Cell, the researchers report they have discovered a new mechanism that regulates the action of K-Ras, a cellular protein that plays an important role in many human cancers. "The general feeling was that we had learned everything about ras that there is to know," says Mark Philips, M.D., Professor of Medicine, Cell Biology, and Pharmacology at NYU School of Medicine, who led the study. "But here is a completely new twist on the story."
The researchers "add a striking new dimension to our understanding of how Ras protein function can be regulated," writes Larry A. Feig, Ph.D., Professor of Biochemistry at Tufts University School of Medicine, Boston, in an editorial accompanying the study.
Ras proteins have captured the interest of cancer researchers since the late 1970s, when the first oncogenes -- genes that cause the transformation of normal cells into cancerous cells -- were discovered. One of those oncogenes was ras. There are three ras genes, and K-Ras is the most important in terms of its impact on human cancer.
K-Ras acts like as a molecular switch. In its normal form, the protein can be turned on and off to control pathways that regulate cell growth. The mutated form, however, is locked in the "on" position, causing cells to grow uncontrollably and, at the same time, turning off programmed cell death, or apoptosis, the process that tells a cell when it is time to die. The result is cancer.
Until recently, K-Ras was thought to function only at the cell membrane, where the protein is permanently anchored in place
Contact: Jennifer Choi
New York University Medical Center and School of Medicine