Abstract
Abstract Background: MicroRNAs (miRNAs) as small non-coding RNAs are regulators of gene expression in tumor development and progression. However, its specific role in metastasis of clear cell renal cell carcinoma (ccRCC) is almost unknown. Therefore, we aimed in defining specific miRNA expression pattern of metastatic ccRCC and identifying cellular functions of specific miRNAs deregulated in metastatic process. Methods: We isolated total RNA of 29 ccRCC samples (including 13 non-metastatic and 16 metastatic tumors) and from 16 metastases using snap frozen tissue. Single channel microarray analysis was performed for a global miRNA expression profiling in 22 ccRCC samples. The validation of the differentially expressed miRNAs in metastatic ccRCC compared to non-metastatic tumor samples and furthermore in metastases of ccRCC was performed by using qRT-PCR. Results: We identified a miRNA expression pattern that distinguishes between metastatic and non-metastatic ccRCC. Furthermore, we found a group of miRNAs with altered expression in early-metastatic compared to late metastatic and non-metastatic tumors. These microarray results were verified by qRT-PCR. By analyzing the expression of four of these differentially expressed miRNAs (26a, 30c, 126, 451) in metastases tissue by qRT-PCR we detected the same expression behavior as in the primary metastatic tumor counterparts. Conclusion: Our findings indicate that miRNAs are involved in the metastatic process. Thus, we were able to identify a specific miRNA expression pattern in metastatic ccRCC. Metastases of ccRCC are characterized by the same expression value of specific miRNAs as the primary metastatic tumor tissue. These investigations showed that specific miRNAs are possible prognostic markers for metastatic disease in RCC patients. Further studies have to define the functional role of the miRNAs in the metastatic process. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1142. doi:10.1158/1538-7445.AM2011-1142
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