Some of the worst news you can get when you have been diagnosed with cancer is that is has spread, a process known scientifically as metastasis. This is where some cells break off from the original tumour and use the circulatory system as a method of transportation to get to and invade tissue in a different part of the body. This makes treatment a lot harder: not only are there tumours at multiple locations, but with current medicine it is nearly impossible to locate and target cancerous cells within the bloodstream. This means they could evade destruction and colonise tissue even after all visible tumours have been treated.
On 9th February 2016 Cancer Research UK sent out a press release detailing one of their most recent breakthroughs: they have identified a mechanism used by breast cancer cells in order to leave blood vessels and invade new tissue within the body. This provides a potential new therapeutic target.
It is well known that tumour cells use blood vessels as a track to migrate to different parts of the body. However, up until now it has been poorly understood how the cells, once in the vessels, can then get through the selective barrier between cells and leave the bloodstream. The new development, from a team lead by Dr Claus Jorgensen at the Institute of Cancer Research in London and Cancer Research UK’s Manchester Institute, has identified a protein that is used by breast cancer cells in order to regulate their movement across the blood vessel walls.
The protein involved, called EPHA2, is a receptor on the surface of the cells that line our blood vessels (endothelial cells) which mediates cell attraction and repulsion. It is now thought that cancer cells can communicate with endothelial cells and use the EPAH2 receptor to control their movement across the barrier between blood and tissue.
The new research shows that, when the receptor is active, the endothelial cells are more attracted to one another and stay packed tightly together, allowing the tumour cells to stay in the confines of the blood vessel and travel through the body. Then, when the tumour cells reach the area of the body they are intended for, they deactivate the receptor, causing the epithelial cells to become more repulsive to one another, allowing the cancer cells to push themselves through the barrier and into the surrounding tissue.
This breakthrough is exciting as it opens up the new possibility that the EPHA2 receptor, with more research, could be used as a pharmaceutical target. If we can figure out how to keep the EPAH2 receptor active at all times it may allow us to be able to prevent cells from crossing the blood vessel wall, stopping cancer from spreading and making more cases curable.