Over expression of the centrosomal protein Cep55 is often cited in gene expression profiles of a variety of tumour types including breast cancer signatures of late stage disease, which have shown to correlate with aggressive subtypes and poor patient outcome. High expression of Cep55 has been associated with increased rates of metastasis and has also been shown to contribute to migration and invasion of lung cancer cells in vitro. To examine Cep55’s role in metastatic progression we depleted Cep55 in the metastatic breast cancer cell line MDA-MB-231. We found Cep55 to be required for cell migration in vitro. Interestingly in mouse xenograft models, Cep55 depletion reduces lung metastatic growth but not primary mammary tumour growth. We hypothesize that Cep55 is likely to be required to interact and activate the PI3K/AKT pathway resulting in increased cellular survival, proliferation and migration in the metastatic setting which is a crucial step in disease progression of carcinomas. Further insights gained into Cep55 function in tumour progression and metastasis will provide potential avenues for novel treatment options for metastatic disease in the future.