Colorectal cancer is closely associated with mutation of the gene encoding the adenomatous polyposis coli (APC) tumor suppressor protein. A role has been defined for APC in the Wnt signaling pathway, in which it is responsible for mediating the degradation of the protein β-catenin. This function is clearly responsible for the tumor suppressor activity of APC. However, other APC functions have been identified, notably involving the cytoskeleton, the loss of which may be involved in shaping the phenotype or contributing to the progression of colorectal cancer. Here we provide an insight into recent developments in the study of APC interactions with cytoskeletal elements.