Abstract
Abstract [Introduction] Endometrial cancer has now become the most common gynaecologic malignancy worldwide. About 80-90 % of endometrial cancer are endometrioid endometrial adenocarcinomas (EEC). MicroRNAs (miRNAs) are short, non-coding RNAs that regulate gene expression by inducing cleavage of the targeted messenger or by inhibiting translation. Our entire study was to mine miRNA signatures involved in EEC tumorigenesis and progression. Here we report a part of the results that is on miRNAs associated with endometrial cancer progression in vitro. [Methods] We examined the expression of 365 mature miRNAs by real-time RT-PCR based plate assays in 52 EEC including 30 advanced- and 22 early-stage tumors, and compared that to 30 normal counterparts. To know about the deregulated miRNAs associated with endometrial cell behavior, miRNA inhibitor and pre-miRNA were used to inhibit up-regulated miRNA and induce down-regulated miRNA in highly invasive endometrial cancer cell line HEC-1A cells. Quantitative TaqMan RT-PCR was performed to measure miRNA levels in cells before and after treatment, respectively. Migration and invasion assays were carried out to evaluate effects of those deregulated miRNAs on invasion of endometrial cancer cells in vitro. [Results] Supervised clustering analysis of global miRNA expression in endometrial caner and normal control identified 17 miRNAs up-regulated and 2 miRNAs down-regulated, respectively, in EEC. When the miRNA expression profiles in advanced stage tumors were compared to those in early stage tumors, 6 miRNAs were significantly over-expressed and one miRNA under-expressed in advanced stage tumors. Cell migration and invasion assay showed the ability of cell migration and invasion was significantly inhibited by anti-miR-7, anti-miR-194, anti-miR-449b and pre-miR-204 in HEC-1A cells in vitro. [Conclusion] Unique miRNA signatures seem to be existed in ECC. Deregulated miRNAs miR-7, miR-194, miR-204 and miR-449b might mediate endometrial cancer progress. These miRNAs are potentially to be developed as novel diagnostic and/or prognostic molecular markers as well as candidate therapeutic targets of EEC. 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 4047.
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