ATM (ataxia-telangiectasia mutated) and ATR (ATM- and Rad3-Related) play a significant role in cell cycle checkpoint function in response to DNA damage, and defects in these genes are associated with tumorigenesis. We have previously demonstrated that > 25% of melanoma cell lines are defective for ATM-dependent cell cycle arrest, the result of over activation of Polo-like kinase 1 (PLK1), a G2/M cell cycle regulator. Melanomas are associated with dysregulated expression of PLK1 and its upstream activators Aurora kinase A (AURKA), BORA and PPP6C. This study is focused on how overexpression of AURKA influences on ATM and ATR cell cycle checkpoint function. Using time-lapse microscopy imaging, I have demonstrated that the ATM, but not ATR imposed G2 phase cell cycle arrest is abrogated in ATM and ATR checkpoint proficient A2058 and A375 cell lines where I have over-expressed AURKA. This was validated by using selective inhibitors for ATM, ATR, Checkpoint kinase 1 and 2 (CHK1 and CHK2). Inhibition of AURKA or PLK1 further demonstrated that ATM dependent checkpoint recovery was provoked via phosphorylation of PLK1 and AURKA. AURKA overexpression did not overcome ultraviolet radiation induced ATR dependent checkpoint arrest. AURKA overexpression reduced the level of WEE1 and increased the level of activated, phospho-Thr210 PLK1 during normal cell cycle progression, and in the G2 phase checkpoint arrest. Over-expression of AURKA also influences DNA damage repair. This provides evidence that dysregulated AURKA can bypass ATM dependent checkpoint arrest in melanoma, and may contribute to genomic instability.