Expression of Aurora kinases in adrenocortical tumors

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 17-28-Adrenal Tumors & Pheochromocytoma
Basic/Clinical
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-27
Raffaele Pezzani*1, Beatrice Rubin1, Maria Verena Cicala1, Monica Salvā1, Maurizio Iacobone1, Salvatore Ulisse2 and Franco Mantero1
1University of Padova, Padova, Italy, 2Univ of Rome, Roma, Italy
Expression of Aurora kinases in adrenocortical tumors

Raffaele Pezzani1, Beatrice Rubin1, Maria Verena Cicala1, Monica Salvà1, Maurizio Iacobone2, Salvatore Ulisse3, Franco Mantero1

1 Endocrinology Unit, Department of Medicine, University of Padova, via Ospedale Civile 105, 35128 Padova, Italy; 2 Endocrine Surgery Unit, Department of Surgical and Gastroenterological Sciences, University of Padova, Via Giustiniani, 2, 35128 Padova, Italy; 3 Department of Experimental Medicine, University of Roma “La Sapienza”, Viale Regina Elena 324, 00161 Roma, Italy.

Background: Both secreting and non-secreting adrenocortical tumors (ACT) are frequently found and are mostly benign, but among them, adrenocortical carcinomas (ACC), although rare, show poor prognosis and metastatic potential. Aurora kinase (AK) family members are serine/threonine kinase 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 adenoma (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 3H thymidine 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 85nM. Furthermore we observed a significant time-dependent reduction in cell proliferation for SW13 cells at 24 and 72h. No appreciable change was perceived in H295R cells.

Conclusions: 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 seems to act only in SW13 cells. Further analysis are needed to substantiate these data.

Nothing to Disclose: RP, BR, MVC, MS, MI, SU, FM

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm