ACTIVATING a liver cell protein that detects pathogens from fungus can make the cells “eat” cancerous cells, researchers in Japan announced in a study published late last month in the Proceedings of the National Academy of Science.
A research group led by Project Researcher Yoshitaka Kimura and Professor Tadatsugu Taniguchi at the University of Tokyo’s Institute of Industrial Science was investigating the process of metastasis, the spread of cancer from one part of the body to another, which is a major cause of mortality in cancer patients. The researchers focused on the liver, because the spread of disease to the liver is common among many kinds of cancers, resulting in a poor prognosis for patients.
The immune system plays a critical role in stemming liver metastasis, but the mechanism by which it does so is largely unknown, the researchers explained in their paper.
The researchers found that Dectin-2, a cell surface protein involved in the recognition of fungal pathogens, promotes the engulfment of cancer cells in the liver by what are known as Kupffer cells. Using mice lacking the Dectin-2 receptor, the scientists were able to demonstrate that the body’s natural immune system plays a role in suppressing cancer development in the liver.
The effect of the Dectin-2 protein is triggered selectively in the liver, the researchers said, since the immune response was not observed in mice with tumor growth under the skin or with lung metastasis.
The researchers also found that MCL, a receptor known to bind with Dectin-2, works synergistically with Dectin-2 to suppress liver metastasis.
“Dectin-2 is well-known for the key role it plays in protecting against disease-causing agents such as the Candida fungus,” said Taniguchi. “I found it very intriguing that the protein serves an important function in eliminating cancer cells as well.”
The research team said that possible extensions of their work could involve searching for other cell proteins in other parts of the body that have a similar effect on cancer cells, which could eventually lead to new treatments for the disease.
The study was carried out in collaboration with scientists from Chiba University, Kyushu University, and Tokyo University of Science.