HOUSTON - Like a bounty hunter returning escapees to custody, a cancer-fighting gene converts organ cells that change into highly mobile stem cells back to their original, stationary state, researchers report online at Nature Cell Biology.
This newly discovered activity of the p53 gene offers a potential avenue of attack on breast cancer stem cells thought to play a central role in progression and spread of the disease, according to scientists at The University of Texas MD Anderson Cancer Center.
Long known for monitoring DNA damage and forcing defective cells to kill themselves, p53 also activates bits of RNA that block two proteins, the researchers found. This prevents conversion of epithelial-differentiated cells, which line or cover an organ, into cells that resemble mesenchymal stem cells when stimulated by the TGF-??growth factor.
Mesenchymal cells are mobile adult stem cells that can reproduce themselves and differentiate into a variety of cell types
"Blocking this conversion from epithelial cell to a mesenchymal cell type is important because that change plays an essential role in cancer metastasis," said senior author Mien-Chie Hung, Ph.D., professor and chair of MD Anderson's Department of Molecular and Cellular Oncology.
Cancer treatment potential
"We found that p53 activates the micro RNA miR-200c, which forces cells that have taken on stem cell traits to revert to epithelial form," Hung said. "Activating this pathway has therapeutic potential to target tumor-initiating cells that have stem cell characteristics."
Research has shown that about 80 percent of all solid tumors begin in the epithelial cells. However, 90 percent of cancer deaths are caused by metastasis, the progression and spread of the disease to other organs.
The epithelial-to-mesenchymal transition (EMT) and its opposite process play important roles in embryonic development. Research has co
|Contact: Scott Merville|
University of Texas M. D. Anderson Cancer Center