Cytoskeleton out of the cupboard: colon cancer and cytoskeletal changes induced by loss of APC

There is evidence that apart from its ability to regulate the transcriptional activity of β-catenin, adenomatus polyposis coli (APC) has β-catenin-independent functions. Is the interaction of APC with cytoskeletal components important for cancer development and progression in the gut? 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 β-catenin-mediated gene transcription in response to Wnt signalling. Loss of APC leads to deregulated β-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?