Abstract 2998: MicroRNA expression signatures in human ovarian tumor progression

Abstract

Differential expression of a number of miRNAs has previously been detected between normal ovaries and epithelial ovarian cancer (EOC). However, miRNA expression signatures have not been demonstrated between primary human ovarian surface epithelial (HOSE) cell, cystadenoma, low malignant potential (LMP) ovarian tumor and ovarian carcinoma as well as fallopian tube. Here, we performed miRNA profiling in normal primary OSE cells, normal fallopian tube and ovarian tumors, including 7 cystadnomas, 6 LMP and 49 ovarian carcinomas, as well as 15 ovarian cancer cell lines and 5 HIOSE cell lines. While deregulated dozen miRNAs were observed in different histological types of cysadenoma, LMP and ovarian carcinoma compared to primary OSE and fallopian tube, there are no significantly common changed miRNAs between serous adenoma and LMP, as well as between mucinous adenoma and LMP. However, 3 miRNAs were co-downregulated and 7 miRNAs were co-upregulated in serous LMP and carcinoma. When comparing mucinous LMP and carcinoma, only 3 miRNAs were co-deregulated. In addition, 3 and 6 miRNAs were co-deregulated in mucinous and serous adenoma and carcinoma, respectively. While miRNA expression patterns are distinct among four histological types of ovarian carcinoma examined, upregulation of miR-221/222 family was found to have significant poor prognosis value in serious carcinoma (p<0.05). These results support the notion that majority of ovarian carcinoma are derived neither from cystadenoma nor from LMP. Further cluster analysis suggests that the serious ovarian cancer may be derived from fallopian tube or/and OSE. Also our data suggest that commonly deregulated miRNAs between adenoma, LMP and carcinoma could serve as not only early markers but also initiation pathogenetic factors in this malignancy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2998.