As a tumor grows, cells can break off it and move around the body, potentially spreading the disease to other organs. Known as metastasis, this process significantly lowers the patient's likelihood of survival, but a new discovery could help doctors tackle it, with researchers form Imperial College London identifying a molecule that shows promise in switching off the process altogether.

With everything from being able to more accurately detect the condition in the prostate, to using antigen-loaded silicon microparticles to help the immune system tackle breast cancer, our understanding of cancer, and our ability to combat it, is constantly evolving. This new Imperial College London study has identified a possible means of switching off the ability of tumor cells to spread around the body, potentially limiting the damage that the disease can do.

Looking specifically at lung and breast cancers, the team was able to determine that a protein, known as MARK4, is responsible for the tumor cells' ability to break away and travel to other parts of the body, through blood vessels or the lymph system. While its not yet confirmed exactly how MARK4 does this, the researchers theorize that the protein is able to alter cells' internal scaffolding, giving them the ability to move around more easily.

As the study continued, the team was able to make another discovery – that a molecule known as miR-515-5p is actually able to switch off the gene that produces MARK4. In so doing, the researchers could, in theory at least, turn off tumor cells' ability to travel around the body.

Putting the theory to the test, the scientists first used lung and breast cancer cells to successfully demonstrate miR-515-5p silencing MARK5 proteins, before moving on to animal studies. By increasing levels of the molecule in mice, the team found that they were indeed able to prevent cancers from spreading.

Spurred on by the positive results of the lab and animal testing, the researchers then looked to human patients, and were able to determine that patients whose tumors exhibited low levels of the silencing molecule, and therefore high levels of the dangerous protein, were less likely to survive the condition. Although not conclusive, this indicates that the mechanism may work in humans, just as it does in mice.

While more research is required, in the long run the work could provide a new means of treating breast and lung cancers, and might even be useful in tackling other forms of the disease.

"In our work we have shown that this silencer molecule is important in the spread of cancer," said senior paper author Professor Justin Stebbing. "This is very early stage research, so we now need more studies to find out more about this molecule, and if it is present in other types of cancer."

The research was published in the journal EMBO Reports.