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Transcriptional Coactivator Drosophila Eyes Absent Homologue 2 Is Up-Regulated in Epithelial Ovarian Cancer and Promotes Tumor Growth

¹ Abramson Family Cancer Research Institute, ² Center for Research on Reproduction and Women's Health, ³ Department of Obstetrics and Gynecology, and ⁴ Department of Genetics and Cell and Molecular Biology Program, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania and ⁵ Department of Obstetrics and Gynecology, University of Turin, Turin, Italy

Requests for reprints: George Coukos, Center for Research on Reproduction and Women's Health, University of Pennsylvania, 421 Curie Boulevard, 1355 Biomedical Research Building II/III, Philadelphia, PA 19104. Phone: 215-746-7798; Fax: 215-573-7627; E-mail: gcks{at}mail.med.upenn.edu.

Epithelial ovarian cancer is the most frequent cause of gynecologic malignancy-related mortality in women. To identify genes up-regulated in ovarian cancer, PCR-select cDNA subtraction was done and Drosophila Eyes Absent Homologue 2 (EYA2) was isolated as a promising candidate. The transcriptional coactivator eya controls essential cellular functions during organogenesis of Drosophila. EYA2 mRNA was found to be up-regulated in ovarian cancer by real-time reverse transcription–PCR, whereas its protein product was detected in 93.6% of ovarian cancer specimens by immunohistochemistry (n = 140). EYA2 was amplified in 14.8% of ovarian carcinomas, as detected by array-based comparative genomic hybridization (n = 88). Most importantly, EYA2 overexpression was significantly associated with short overall survival in advanced ovarian cancer (n = 99, P = 0.0361). EYA2 was found to function as transcriptional activator in ovarian cancer cells by Gal4 assay and to promote tumor growth in vivo in xenograft models. Therefore, this study suggests an important role of EYA2 in ovarian cancer and its potential application as a therapeutic target.

Key Words: Ovarian Cancer • Drosophila Eyes Absent Homologue 2 • Gene Expression

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