Researchers at the OU Cancer Institute have identified a new gene that causes cancer. The ground-breaking research appears Monday in Nature’s cancer journal Oncogene.

The gene and its protein, both called RBM3, are vital for cell division in normal cells. In cancers, low oxygen levels in the tumors cause the amount of this protein to go up dramatically. This causes cancer cells to divide uncontrollably, leading to increased tumor formation.

Researchers used new powerful technology to genetically “silence” the protein and reduce the level of RBM3 in cancerous cells. The approach stopped cancer from growing and led to cell death. The new technique has been tested successfully on several types of cancers – breast, pancreas, colon, lung, ovarian and prostate.

“We are excited about this discovery because most cancers are thought to come from mutations in genes, and our studies, for the first time, have shown that too much of this type of protein actually causes normal cells to turn into cancer cells,” said Shrikant Anant, Ph.D., a cancer biologist at the OU Cancer Institute and principal investigator on the project.

Anant said they found RBM3 protein in every stage of many cancers, and the amount of protein increased as the cancer grew. The protein helped the cancer grow faster, avoid cell death and was part of the process that formed new blood vessels to feed the tumor.

“This process, called angiogenesis, is essential for tumor growth and suggests that targeting RBM3 may be an extremely powerful tool against many and perhaps all solid tumors,” Anant said.

A quarter of the funding for the cancer research comes from an $800,000 grant from the National Institutes of Health with remaining funds from the University of Oklahoma College of Medicine. The next step for Anant, Dr. Courtney Houchen and their research team at the OU Health Sciences Center is to develop agents that block the protein function in a variety of cancers. Researchers expect to start clinical trials at OU in about five years.

http://www.ouhsc.edu/article-display.asp?idnum=1232