One of the big challenges with cancer therapy is how to keep the disease under control when it starts to spread round the body. In a potential boost for tackling cancer, scientists have identified the mechanism by which a cancer gene promotes metastasis.
Cancer metastasis
The most deadly aspect of cancer is its ability to spread round the body, or metastasize. When localized in a specific area such as a tumour, it is relatively easier to tackle. Surgeons can remove it or the target area can be bombarded with drugs. But once it spreads through lymph and blood vessels to many other parts of the body, treatment becomes all but impossible.
At some point somewhere, there is a signal or set of signals that sets the cancer off on its deadly mission. Snuff out these signals and the cancer stays local.
Melanoma gene
Scientists from the Virginia Commonwealth University Institute of Molecular Medicine and VCU Massey Cancer Center have made bold strides in this direction. They have discovered how a gene, melanoma differentiation associated gene-9/syntenin (mda-9/syntenin) interacts with a signalling protein to metastasize in melanoma cells.
Genetics of metastasis
Understanding more about the basic genetics underlying metastasis should lead to the development of the next generation of anti-metastatic drugs. Not only for melanoma but for other cancers too.
The researchers studied cancer cells in the lab and focused on mda-9/syntenin. It was already known that it alters biochemical pathways leading to metastasis. But how it was doing this was unknown. Not anymore.
The gene is 
involved in an incredibly complex chain of cellular events.
1) It physically interacts with a signalling protein called c-Src that's involved with tumour growth and metastasis. The gene can activate the expression of c-Src.
2) When this happens there's an increase in the formation of FAK/c-Src signalling complex, which results in increased cancer cell motility and metastasis.
Stopping metastasis
The research was published on September 29 in the Early Edition of the Proceedings of the National Academy of Sciences and the researchers claim that metastasis could be stopped if the mda-9/syntenin and c-Src interaction is disrupted.
"By disrupting the interaction between mda-9/syntenin and c-Src, it may be possible to prevent metastasis by blocking those signal changes necessary for this process," said Paul B. Fisher,, M.Ph., Ph.D., director of the VCU Institute of Molecular Medicine
The team's next task is to go back to the lab and experiment with small molecule drugs to see if they can disrupt this gene-protein interaction.