A Jackson Laboratory research team led by Professor Lenny Shultz, Ph.D. (pictured), reports that a protein involved in wound healing and tumor growth could be a potential therapeutic target.
In one of nature’s mixed blessings, the mechanisms that work to heal cuts and wounds, rebuilding damaged cells, can also go out of control and cause cancer. But understanding those mechanisms could lead to new ways of stimulating healing in wound patients and dialing back cancerous proliferation.
iRhom2 is normally a short-lived protein that controls a cascade of events involved in wound healing as well as tumor growth. By introducing mutations in Rhbdf2, the gene that encodes the iRhom2 protein, the researchers extended the protein’s duration and wound-healing power. And while the altered protein also contributed to the growth of already-present tumors, it did not trigger the spontaneous development of new tumors.
According to Shultz, epidermal growth factor receptor (EGFR) signal transduction plays a major role in growth, proliferation, and differentiation of mammalian cells. “This study demonstrates the significance of mammalian iRhoms in regulating an EGFR signaling event that promotes accelerated wound healing and triggers tumorigenesis,” Shultz explains. “Given their ability to regulate EGFR signaling in parallel with metalloproteases, iRhoms can be potential therapeutic targets in impaired wound healing and cancer.”
Illustration: The Jackson Laboratory.
The Jackson Laboratory News Release (05/12/14)
Science Daily (05/12/14)
Abstract (Proceedings of the National Academy of Sciences of the United States of America; (2014))