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Protein that promotes cancer cell growth identified
Date:7/24/2009

e-blot assays to demonstrate that reconstituting the Caspase-8 deficient cells with Caspase-8 with mutations in the RXDLL domain did not result in EGF signaling. This suggests that Caspase-8 mediates signaling through the RXDLL domain. The scientists had previously shown in another study that Caspase-8 associates with Src, a protein known to be involved in cancer cell proliferation. In this study they showed that interruption in this association disrupts EGF signaling indicating that Caspase-8 exerts EGF signaling through Src.

Cancer results from excessive cell division and reduced cell death. A number of cell death proteins are missing from human tumors, allowing cancer cells to ignore the cues that keep their growth in check. Cells that can evade apoptosis have a clear growth advantage. Because Caspase-8 is involved in programmed cell death, it would seem that reducing Caspase-8 in cancer cells would provide a growth advantage. However, this is rarely observed in human cancers.

By providing a more complete understanding of the molecular mechanisms involved in cancer cell proliferation and migration, these results point to Caspase-8 as a novel therapeutic intervention point for treating multiple types of human cancers.


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Contact: Josh Baxt
jbaxt@burnham.org
858-795-5236
Burnham Institute
Source:Eurekalert

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