Cervical cancer remains a significant global healthcare issue. Despite the introduction of the prophylactic HPV vaccine, it will likely be another 10-20 years before this vaccine causes a significant difference in cervical cancer rates. Recent in vitro and in vivo studies have demonstrated that inhibition of the mitotic regulator Aurora kinase A with the small molecule inhibitor Alisertib, results in selective killing of HPV-positive cancer cells when compared to HPV-negative cancer cells, and shows great potential as a cervical cancer therapy. Alisertib was initially described in the literature as a selective Aurora Kinase A (AURKA) inhibitor, however the phenotype of Alisertib treated cervical cancer cells appears to more closely resemble the phenotype of Aurora Kinase B (AURKB) inhibited cells. In order to determine the mechanism by which Alisertib selectively targets HPV-positive cancer cells it is important to determine whether its effect is due to the inhibition of AURKA alone or whether there is also a significant degree of AURKB inhibition involved. To investigate this we have investigated the in vivo inhibition of AURKA and AURKB in HeLa cells when treated with Alisertib. AURKA and AURKB activity will be assessed by measuring levels of the downstream substrates phospho-Aurora A (Thr288) and phospho-histone H3 (Ser10), respectively. The relative inhibition of AURKA and AURKB will be compared to that in HeLa cells treated by a selective AURKA inhibitor (CCT24491), a selective AURKB inhibitor (ZM447439) and a pan Aurora Kinase inhibitor (AMG900). The effects of these drugs on mitosis and apoptosis were also monitored. This study will determine whether the efficacy of Alisertib is solely due to Aurora A inhibition or a inhibition of a combination of targets, and determine whether the HPV-dependent killing a is unique feature of Alisertib or common to pan Aurora kinase inhibitors.