Research Shows Tumor-
Supressing Protein Action

NEW YORK (Reuters Health) - Keeping the tumor-suppressing protein p53 in the cell's nucleus is critical for helping it repair cancer-causing DNA damage. Now scientists say that the same factors that cause DNA damage also change p53 in a way that keeps it at the damage site.

Too much p53 in the nucleus would arrest the growth of the cell or even result in its death, Dr. Yue Xiong, from University of North Carolina at Chapel Hill, told Reuters Health. So under normal conditions, p53 rapidly exits the nucleus of cells.

Writing in the June 8th issue of Science, Xiong and colleague Dr. Yanping Zhang wondered what keeps p53 from exiting a cell's nucleus so it can repair damage after insults such as radiation exposure.

By using modified forms of p53, the authors pinpointed an area along the protein that was necessary to expel it from the nucleus. Mutations that changed this area kept the protein inside the nucleus.

Similarly, DNA damage results in changes to this same area of p53. When damage occurs, certain bulky molecules attach themselves to the p53 protein. And it is these molecules that prevent p53's exit from the nucleus.

These results highlight a previously unrecognized method that cells use for preventing cancers, wherein the damage itself activates p53 protein and keeps it in the nucleus until the repair is under way, the researchers conclude.

Understanding how p53 is activated is vital to developing new cancer therapies that use the natural tumor-suppressor, according to Xiong.

``Undoubtedly, the challenge now is to tease apart the intricate circuitry that controls...p53,'' Drs. Vanesa Gottifredi and Carol Prives, from Columbia University, in New York, write in a related commentary.

SOURCE: Science 2001;292:1910-1915.

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