In a new study in mice, researchers overcame a process by which cancer co-opts a fundamental protein into protecting it against the body’s defenses.
For cancer to spread, the cells that take off into the bloodstream must find a tissue that will permit them to thrive. They don’t just go looking, though. Instead, they actively prepare the tissue, in one case by co-opting a protein that suppresses defenses the body would otherwise mount. In a new study, scientists report that by wresting back control of that protein, they could restore multiple defenses in the lungs of mice, staving off cancer’s spread there.
“Cancers are known to have the ability to co-opt or evade host anti-tumor responses,” said Dr. Jack A. Elias, dean of medicine and biological sciences at Brown University and corresponding author of the study in the Nature journal Scientific Reports.
A key protein that apparently becomes co-opted is Chitinase 3-like-1 (CHI3L1), which has a natural purpose in a wide array of organisms where it helps to fight infections and stimulates tissue healing. However, it is also susceptible to going awry where it contributes to the generation of a variety of diseases. In human diseases like idiopathic pulmonary fibrosis it mounts an overzealous response that leads to pulmonary scarring, and in diseases like asthma it sustains a harmful immune response. People have a directly analogous version of the protein called YKL-40 and, in patients with cancer, high levels of its expression correlate strongly with advanced cancer spread and a poor prognosis