New Role for P53 Gene

Utilizing a mouse model, they demonstrated that lack of the mediator makes the mice vulnerable to the development of cancer. With this finding, the scientists are providing a means to better understand the molecular processes that regulate tumor development.

The billions of cells that compose the body are being replaced daily: old cells die and new ones are made. In the course of this process, each cell goes through a well-organized series of phases. Firstly, the DNA in the cell nucleus is copied. Then the nucleus divides itself in half; next, the complete cell divides, and the daughter cells grow into totally new cells. Because it is vital for this cell cycle to run flawlessly, various control points have been established to enable the cell to regulate the stability of the DNA. If the DNA becomes damaged, the cell cycle will come to a stop.

The p53 protein is responsible for halting the cell cycle. Typically, this occurs at the end of the growth phase; however, if the DNA has been damaged or if other problems arise, p53 can also initiate programmed cell death. Because p53 can stop the additional growth of cells, this protein plays a fundamental role in suppressing the development of tumors and stopping the onset of cancer. When cancer occurs, the p53 protein is turned off, either through an alteration or mutation in the gene itself, or through modified activity of the proteins that control p53 or that influence its activity.

Researchers at Flanders Interuniversity Institute for Biotechnology (VIB; Ghent, Belgium; www.vib.be) have discovered that the protein Ptprv works in conjunction with p53. In specific instances, p53 directly influences the Ptprv production. In the case of DNA damage, Ptprv plays a major role in stopping the cell cycle and also helps block the development of tumors. This important role for Ptprv has been demonstrated using mouse models. Although the researchers have illustrated its role in the development of cancer, the actual function of Ptprv is unknown.

After exposure to carcinogens, mice that lack Ptprv develop cancer much more quickly than healthy mice do. The results of this study reveal that Ptprv is a major player in preventing and counteracting cancer. Further studies should demonstrate whether Ptprv can be a potential application for the treatment of cancer. The study was published in the August 18, 2005, online issue of the EMBO Journal.




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Flanders Interuniversity Institute for Biotechnology