Abstract
Mutation of APC (adenomatous polyposis coli) is a common factor in most colorectal cancers. APC has many functions, the most prominent is its capacity to regulate beta-catenin-mediated gene transcription in response to Wnt signalling. Loss of APC leads to deregulated beta-catenin and this is intimately linked with tumour formation. However, recent evidence indicates that the interaction of APC with the cytoskeleton might also contribute to tumour initiation and progression. How does APC interact with the cytoskeleton and how could this play a part in colorectal tumorigenesis?
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