Writing in the Nov. 17 issue of the Journal of the National Cancer Institute, scientists in the Ohio State University Comprehensive Cancer Center (OSUCCC) note that the protein, called Pirh2, when overexpressed, diminishes the activity of p53 possibly the most powerful tumor suppressor in the entire genome. When it functions normally, p53 regulates several critical cellular processes, including cell growth and death, DNA repair and angiogenesis, the formation of new blood vessels. Studies show that p53 mutation is common, occurring in at least half of all cancer.
"The p53 gene is possibly the most important 'manager' in a cell. When it's not working properly, it can be disastrous," says Miguel Villalona, associate professor of internal medicine in the Ohio State University College of Medicine and Public Health and senior author of the study. Villalona says that this is the first time Pirh2 has been implicated in the loss of p53 function in tumors.
Villalona and his colleagues identified the link between Pirh2 and the development of cancer by evaluating Pirh2 expression in human and mouse lung tumor samples and comparing it with Pirh2 expression in normal tissue from the same samples. They found that Pirh2 expression was higher in 27 of 32 (84 percent) of human lung cancers and in 14 of 15 (93 percent) of mouse tumors than it was in the normal tissue.
"This is the first demonstration that Pirh2 expression is elevated in patients' tumors and supports the notion that it may be an important molecule in the development of lung cancer, says Gregory Otterson, associate professor of internal medicine in the OSU College of Medicine and Public Health and co-author of the study.