A new Arizona State University research study led by Biodesign Institute executive director Raymond DuBois, M.D., Ph.D., has identified for the first time the details of how inflammation triggers colon cancer cells to spread to other organs, or metastasize.
|Scooped by Graham Player Ph.D.|
A study led by Raymond DuBois, M.D., Ph.D., a leader in colorectal cancer research for more than two decades, has been exploring the risk factors between chronic inflammation and cancer, including colorectal cancer.
The research team was able to show how a colon cancer tumor could outwit its host, using an inflammatory mediator to expand its cancer stem cells in order to seek out other organs. They showed a direct link between the pro-inflammatory mediator prostaglandin E2 and increased colorectal cancer stem cells.
Prostaglandin E2 is the most abundant pro-inflammatory bioactive fat, or lipid, found in colon, lung, breast, head and neck cancers. When high levels of PGE2 are found in cancer, it often indicates a poor prognosis.
"The normal role of PGE2 is to come to the rescue when you do something like cut your finger," said DuBois. "It attracts the body's immune cells and stimulates pathways that heal the wound site. The level of PGE2 goes up and then goes down within a few days of healing the wound.
But in cancer, the cells keep making PGE2 chronically, so it's like this wounding process that never heals. In doing so, it generates these cancer stem cells that promote cancer progression and metastatic spread."
DuBois' research team proved that when PGE2 binds to its receptor on the surface of the cancer cell, PGE receptor 4, or EP4, it triggers a signaling cascade for cancer stem cells to renew, differentiate and eventually become resistant to chemotherapy.