Protective gene for colorectal cancer identified
Scientists have identified a tumour-suppressing gene called DCC gene (Deleted Colorectal Cancer), which protects against the onset of cancer by causing the death of cells that become cancerous.
The research team at Lyon has also developed an animal model carrying a mutation of the DCC gene. Mice carrying the mutation develop tumours, because this gene can no longer induce the death of the cancer cells. This discovery could lead to the development of a new targeted cancer treatment that aims to reactivate the dying of cancer cells.
The team led by Patrick Mehlen, Director of the DEVweCAN 'Laboratory of Excellence' at the Lyon Cancer Research Centre (CNRS/Inserm/Centre Leon Berard/Universite Claude Bernard 1), studies the cell death process (apoptosis) and, in particular, the mechanism that makes the cells understand that they should initiate a self-destruction process when they become abnormal.
Mehlen's team suggested that this mechanism could operate via sentinels located on the surface of cells, which examine their environment. The scientists named these sentinels 'dependence receptors'. In this study, the team showed that the DCC gene (Deleted Colorectal Cancer), which codes for a 'dependence receptor', protects the organism from the onset of cancer by causing the death of cells that become cancerous.
The researchers used a mouse model where the DCC gene has been genetically modified. The mutation of this dependence receptor prevents the induction of apoptosis. When the DCC gene is eliminated by mutation, the mouse spontaneously develops colon cancer.
"The organism is naturally protected from the development of cancers thanks to the presence of this tumour-suppressing gene," explained Mehlen. "Unfortunately, certain cancer cells escape from this control by blocking this 'dependence receptor' mechanism. That is how we know that the DCC gene is extinguished in most human cancers," he added. The results of this study have been published as a Letter in the 11th December 2011 issue of the journal Nature.