Cancer's immune system 'cloaking device' uncovered
A new study has furthered scientists' understanding of how cancer cells evade detection by the body's immune system.
Scientists have known for several years that cancer cells can cloak themselves with a protective layer of special blood cells, called platelets, to enable them to spread throughout the body.
But exactly how the cancer cells recruit this cellular 'cloaking device' has remained a mystery.
Now, researchers at Japan's University of Yamanashi have found that a protein found on the surface of platelets - cells which are required for blood clotting - allows them to stick to the cancer cells.
The finding may lead to new ways to prevent cancers from spreading.
Katsue Suzuki-Inoue, associate professor of medicine at the university, explained: "In order to spread, cancer cells release chemicals that make neighbouring platelets aggregate and surround the cancer cells, helping them evade the immune system and allowing them to bind to the blood vessels' inner linings.
"We have discovered how one of these chemicals, called podoplanin, binds to the platelet cells and stimulates their aggregation. Although podoplanin has been known since 1990, how it induces platelet cell aggregation has been a mystery - until now."
The researchers discovered that podoplanin binds to a receptor on the surface of platelets called CLEC-2, rather like a key fitting into a lock.
They confirmed this finding by engineering platelet cells so that the CLEC-2 receptors on their surface would be unable to bind with podoplanin. As expected, platelet aggregation was completely prevented, confirming CLEC-2's role in platelet aggregation.
Ms Suzuki-Inuoue commented: "We were pleasantly surprised. After all these years, we finally found the long-missing protein to which podoplanin binds to promote platelet aggregation."
She continued: "Our study clearly shows that podoplanin on the surface of tumour cells induces platelet aggregation by interacting with CLEC-2 on the surface of platelet cells.
"Preventing CLEC-2 and podoplanin from binding to each other may be a good therapeutic way of preventing tumour metastasis."
In addition, the researchers believe that the interaction may be involved in the formation of new blood vessels which are required to fuel tumour growth, suggesting that preventing podoplanin from binding with CLEC-2 may also limit tumour growth.
The researchers are now attempting to develop antibodies that will bind with podoplanin, preventing it from being able to bind to platelet cells.