The findings have altered the perception of the way cell signalling molecules, such as growth factor and cell positioning receptors, communicate and regulate processes such as cell adhesion and motility.
Researchers at Monash University and the Sloan Kettering Cancer Centre in New York discovered the structure of the molecular switch that controls communication between tumour cells.
The "switch" involves a cell-surface protease called ADAM 10 that regulates the signals that promote tumour growth and motility of cancer cells.
Understanding the structure of the ADAM 10 molecule provides the basis for developing pharmaceutical drugs to inhibit tumour growth and metastasis - the spreading of cancerous tumour cells throughout the body.
"While the critical role of ADAM10 in tumour growth and spreading was clear for a long time, we were unaware how ADAM10 achieved its control on the function of important cell surface molecules, such the Eph and Ephrin cell positioning proteins," said Dr Martin Lackmann from Monash's Department of Biochemistry and Molecular Biology.
The team discovered that ADAM10 specifically recognised only Eph and Ephrin molecules that were actively engaged in signalling.
By manipulating the ADAM structure molecular recognition and arrest signalling could be interfered with.
"Being able to regulate the communication between these cell surface molecules, which are found at high levels in many human cancers, by preventing the function of ADAM, may actually stop the growth and spread of tumours," added Lackmann.
The findings are published in the latest issue of the international journal, Cell.