The Adenomatous Polyposis Coli (APC) tumor suppressor gene is mutated in most familial and sporadic colorectal cancers and encodes a large cytoplasmic protein that is implicated in cell migration, cell adhesion, and proliferation. APC binds directly to microtubules and lack of APC leads to defective mitotic spindles and aneuploidy due to missegregation of chromosomes. APC is well characterized as a scaffolding protein, binds to β-catenin, and is involved in the regulation of its intracellular concentration. Disease-associated mutations tend to be clustered in a small region designated the mutation cluster region (MCR) and result in a truncated protein product.
