Expression of Aurora kinases in adrenocortical tumors

Background: Both secreting and non-secreting adrenocartical tumors (ACT) are frequently found and are mostly benign, but among them, adrenocortical carcinomas (ACC), although rare, show poor prognosis and metastatic potential. Auora kinase (AK) family members are serine/threonine kinases involved in the regulation of mitosis.Aim: To investigate the expression of Aurora kinase A, B, C (AKA, AKB, AKC) in adrenocortical tumors and to evaluate the pan-Aurora kinase inhibitor, MK-0457, in adrenocortical cell lines.Materials and methods: 12 ACT were analyzed: 4 ACC, 3 aldosterone producing adenomas (APA), 3 cortisol producing adenomas (CPA) and 2 non-secreting adenomas (NSA). Also 3 normal adrenal tissues and SW13 and H295R cells were studied. All the samples were evaluated by quantitative RT-PCR for AURKA, AURKB, AURKC. MTT test and 3Hthymidine assay were performed in SW13 and H295R cells after treatment with MK-0457. Results: All tissues and cell lines expressed AKA, AKB and AKC. ACC samples overexpressed AKA and AKB, while among ACT only CPA showed increased AKA. MK-0457 inhibited SW13 cell viability at 72h with IC50 of 85 nM. Furthermore we observed a significant time-dependent reduction in cell proliferation for SW13 cells at 24 and 72h. No appreciable change was perceivedin H295R cells.Conclusion: our preliminary results demonstrated AKA, AKB and AKC expression in ACT. AKA overexpression in ACC may suggest the potential anti-mitotic effect of AK inhibitor in adrenocortical cells. Nevertheless MK.0457 seens to act only in SW13 cells. Further analysis are needed to substantiate these data.