A study using a mouse model of mammary cancer shows that loss of a specific ‘dependence’ receptor, which controls cell survival and death (apoptosis), promotes metastasis formation.
These findings are published in Nature this week and support the tumour-suppressing role of this receptor.
The deleted in colorectal cancer (DCC) gene encodes a dependence receptor and, as its name suggests, is frequently deleted in colorectal cancers and many other cancers.
Anton Berns and colleagues constrain its function as a tumour suppressor gene in a mouse model of mammary carcinoma with mutant DCC.
They demonstrate that loss of DCC leads to a loss of pro-apoptotic activity and enhanced tumour cell survival.
These data indicate that loss of DCC function is not selected for in primary tumour development but that its loss facilitates metastasis.
DCC-deficient metastases have been associated with a worse prognosis and a higher risk of recurrent disease in some cancers.
Source: Nature
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