Researchers have isolated a protein that appears to encourage cell movement when tumours begin to spread to other parts of the body opening up the way for a drug that could block the beginning of this dangerous process, or stop it once it starts.
The discovery is all the more illuminating, as this protein is known to be a key factor in the glue that holds cells together in the normal biochemical processes of the human body.
"Our data show that this one protein, p120 catenin, is a key player in both suppressing invasion and promoting it," commented the study's senior author, Panos Anastasiadis, a Mayo Clinic cancer researcher.
"This is very exciting because the findings open up a whole new field of discovery for novel therapeutics that should be applicable to most types of tumours."
The study examined how the protein interacted with other proteins within cancer cells, especially Cadherin goes through a cell membrane, sticking to other cadherin proteins on adjacent cells once outside.
On the inside of the cell membrane, cadherins bind, chain-like, to catenins, and catenins, in turn, regulate a cell's shape and function.
One type of cadherin is E-cadherin, which provides connections between epithelial cells to form a barrier-like layer covering the inside of organs and body cavities as well as the outer skin of humans. E-cadherin holds a human's cells and tissues together.
The other cadherins featured in this study belong to the mesenchymal group and provide a looser bond between the cells that populate the connective tissue.
"Collagen usually provides the strength to the connective tissue, so tight cell-cell adhesion is not that important," said Anastasiadis.
During human development or wound repair, epithelial cells need to travel to other areas, and to do this they undergo a process known as "epithelial-mesenchymal transition" (EMT).
The cell reduces its production of E-cadherin proteins and increases expression of mesenchymal cadherins, thus effectively loosening the anchors that keep the cell bound to its neighbours.
The problem is cancer also uses this strategy in order to spread. When the function of E-cadherin is lost in a cell, it can break free from its neighbours and travel to settle elsewhere.
"This means that E-cadherin normally helps suppress invasion," commented Anastasiadis.
The investigators say that further research is needed to see if p120 functions the same way in living tissue as it does in laboratory cell culture, and they add that other "pathways" are likely involved in the transition to metastasis.
But if the results continue to hold up it might be therapeutically possible to selectively shut down the pro-invasive function of p120 on mesenchymal cadherins while keeping the pro-adhesion function of p120 in normal epithelial cells.
"We have provided a better understanding of the processes involved in the initiation of tumour spread, and it is this process that we all seek to shut down," Anastasiadis concluded.
The study, published in the Sept. 18 online issue of the Journal of Cell Biology.