Scientists from University of Illinois at Chicago have identified a novel mechanism that may help prevent clot formation and inhibit cancer spread.
They claim to have discovered how cells in the body flatten out as they adhere to internal bodily surfaces, the first step in a wide range of important processes including clot formation, immune defense, wound healing, and the spread of cancer cells.
Clots that form in blood vessels can lead to heart attack and stroke.
According to lead researcher Xiaoping Du, to form clots, platelets flatten out to seal the wound and to bind to each other, a process called "spreading." Spreading is the first step in a number of cell processes.
"Understanding these fundamental processes has the potential to allow us to develop drugs to treat thrombosis, stroke and heart attack," said Du.
For cells to move, they must adhere and spread onto the extracellular matrix, a scaffolding of fibres that supports cells. Only then is the cell able to crawl along - whether it be an immune cell moving toward a wound, or a cancer cell invading neighbouring tissue.
Adhesion to the extracellular matrix is mediated by cell receptors called integrins.
The research team "found the mechanism for the transmission of the signal to spread" by the integrins, he said.
The integrin molecule spans the cell membrane, with a portion of the integrin inside the cell and another part outside.
When the outside part of the integrin molecule binds to the matrix, a signal is sent inside the cell via a G protein, a type of protein involved in cell signalling but that was not previously known to interact with integrins.
Du and his colleagues found that the G protein G-alpha-13 binds to the inner side of the integrin molecule when the outside portion binds to the matrix.
G-alpha-13 then inhibits a molecule called RhoA, which allows the cell to flatten out and spread onto the matrix.
The new discovery may lead to drugs that could stop cancer cells from migrating.
The study is published in journal Science.