Epithelial ovarian cancer is the fifth leading cause of cancer-related death among woman and has the highest case-fatality rate among gynecologic cancers. Recently, microarray based high-throughput studies have characterized the genomics of epithelial ovarian cancer. These studies have revealed extensive DNA copy number alterations with large areas of gene amplification. There are however little data identifying the genes critical for the clinicopathologic characteristics of this tumor. Here, we describe an analysis of 11q14 amplicon which has been found in 25% of serous ovarian cancers. Among the genes in the 11q14 amplicon we validate an increased DNA copy number of SYTL2 in patient samples and show that this gene has the strongest negative prognostic power. Ectopic overexpression of SYTL2 in ovarian cancer cell lines A2780 and A224 showed increases in cell proliferation, colony formation, migration and invasion in vitro. In nude mice xenograft models, SYTL2 expression in A2780 cells resulted in increased tumor formation. SYTL2 may act through a novel mechanism by enhancing the secretion of Wnt-3a while having minimal effects on its expression. In summary, our data suggest SYTL2 has oncogenic effcst in ovarian cancer and may contribute to the progression of the disease.

Citation Format: Sung-hoon Kim, Samuel C. Mok, Wei Wei, Vathipadiekal Vinod, Gayatry Mohapatra, Michael Birrer. Aberrantly up-regulated synaptotagmin-like 2 (SYTL2) promotes tumorigenesis of ovarian cancer cells . [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3001. doi:10.1158/1538-7445.AM2013-3001