It is implicated with important processes during mitosis and meiosis whose proper function is integral for healthy cell proliferation.

The Aurora kinase A is associated with centrosome maturation and separation and thereby regulates spindle assembly and stability.

As the cell cycle progresses, concentrations of Aurora A increase and the kinase associates with the mitotic poles and the adjacent spindle microtubules.

Though the cell cycle continues even in the absence of sufficient γ-tubulin, the centrosome never fully matures; it organizes fewer aster microtubules than normal.

[8] In the case of the former, it has been suggested that Aurora A cooperates with the kinase Nek2 in Xenopus to dissolve the structure tethering the cell's centrosomes together.

In the absence of Aurora A mad2, a protein that normally dissipates once a proper kinetochore-microtubule connection is made, remains present even into metaphase.

Though the exact mechanism by which Aurora A aids cytokinesis is unknown, it is well documented that it relocalizes to the mid-body immediately before the completion of mitosis.

[10] Intriguingly, abolishment of Aurora A through RNAi interference results in different mutant phenotypes in different organisms and cell types.

[10] For example, deletion of Aurora A in C. elegans results in an initial separation of the cell's centrosomes followed by an immediate collapse of the asters.

[8] And in Drosophila, flies without Aurora A will effectively form spindles and separate but the aster microtubules will be dwarfed.

The MOS protein accumulates until it exceeds a threshold and then transduces the phosphorylation cascade in the map kinase pathway.

It has been suggested that the fluctuations, or phases, of Aurora A activation are dependent on a positive-feedback mechanism with a p13SUC1-associated protein kinase[10] Aurora A is not only implicated with the translation of MOS during meiosis but also in the polyadenylation and subsequent translation of neural mRNAs whose protein products are associated with synaptic plasticity.

[7] Aurora A has also been shown to be involved in the Epithelial–mesenchymal transition and Neuroendocrine Transdifferentiation of Prostate Cancer cells in aggressive disease.