BACKGROUND: Medulloblastoma comprises approximately 20% of all primary pediatric 
brain tumors. Despite recent advances, the survival rate for high-risk patients 
and the morbidity associated with these treatments remains suboptimal. To 
improve outcomes and decrease morbidity, more targeted therapy is required. One 
possible target is the Aurora Kinase family. The objective of this study was to 
evaluate the impact of Aurora Kinase A inhibition in medulloblastoma cell lines.
PROCEDURE: Cell proliferation was measured using an MTS assay after adding an 
Aurora Kinase inhibitor (C1368) at different concentrations. Cell cycle analysis 
was carried out by Flow Cytometry using propidium iodide (PI). RNAi experiments 
were performed using siRNA oligonucleotides. Luciferase experiments were carried 
out using the Cignal Finder 10 Pathway Reporter Arrays.
RESULTS: Inhibition of Aurora Kinase A induces cell death in medulloblastoma 
cells and lowers the IC(50) of other chemotherapeutic agents (etoposide and 
cisplatin) used in medulloblastoma treatment. Cell arrest at G2/M phase was 
significantly increased in medulloblastoma cell lines treated with C1368 Sigma 
at IC(30) or transfected siRNA. Inhibition of Aurora Kinase A resulted in 
decreased activity of pro-proliferative signaling pathways including Wnt, Myc, 
and RB as measured by luciferase reporter assays.
CONCLUSIONS: These data indicate that inhibition of Aurora Kinase A inhibits 
cell growth in medulloblastoma through inhibition of pro-proliferative signaling 
pathways Wnt, Myc, and RB. Additionally, combining Aurora Kinase A inhibition 
with other chemotherapeutic agents significantly lowers their IC(50), which make 
it a promising small molecule target for medulloblastoma therapy.