Adenomatous Polyposis Coli (APC) is a multifunctional tumour suppressor protein, contributing to pathways in normal cell growth and differentiation. APC gene mutation is one of the earliest events in the progression of colorectal cancer (CRC), and typically gives rise to a truncated protein lacking C-terminal sequences, initiating deregulation of key cellular pathways. This thesis describes a new role for APC in mitochondrial transport. Silencing of wild-type APC by siRNA induced a redistribution of mitochondria from the cell periphery to the perinuclear region. Subsequently, novel interactions for APC were identified at the mitochondria with kinesin-motor complex proteins Miro/Milton. These interactions were mapped to the C-terminus of APC, correlating with defective mitochondrial transport and loss of Miro/Milton binding in CRC cells, which were restored by reconstitution of wild-type APC. Analysis by live cell imaging showed that loss of APC slowed the frequency of mitochondrial anterograde transport towards the cell periphery. It is proposed that APC drives mitochondria to the membrane to supply energy required for directed cell migration, a process disrupted in CRC. This opens up a new route through which CRC-associated APC mutations may contribute to carcinogenesis.