The gene encoding the adenomatous polyposis coli protein (APC) is mutated in most colon cancers. The major role of APC is thought to be as a scaffold for a protein complex that regulates the phosphorylation and thus degradation of β-catenin in the WNT signalling pathway (Huelsken and Behrens, 2002). However, there is increasing evidence that dysregulation of β-catenin is not the only effect of mutations in APC relevant to the development of cancer and that interactions between APC and cytoskeletal proteins are also important.
Cancer-associated mutations in APC usually lead to the expression of N-terminal fragments. This region of the APC protein contains heptad repeats that are predicted to form coiled-coil domains and might be involved in oligomerisation (Joslyn et al., 1993). The N-terminal region of APC also contains two nuclear export signals (NES) that are required for shuttling of APC between the nucleus and cytoplasm...
