We were thus led to explore the potential role of lncRNAs in RCC

To the best of our knowledge, there are only three works reporting microarray data on the expression of lncRNAs in RCC. In 2008, Brito et al.first reported a subset of downregulated intronic noncoding RNAs in six patients with clear cell RCC. More recently the same groupperformed another microarray experiment and uncovered a signature of differentially expressed intronic lncRNAs in 11 ccRCC patients. In 2012, Yu et al.published the lncRNA expression signatures of six ccRCC patients determined through microarray. In the present study, to identify aberrantly expressed lncRNAs in RCC we compared the microarray expression profiles of lncRNAs from cancer tissues of five RCC patients relative to those of matched healthy tissues. Two of the thousands of deregulated lncRNAs we identified were further evaluated in 70 pairs of matched tumor/non-tumortissues via quantitative reverse transcription polymerase chain reaction. Our results may help to find new biomarkers in RCC. Over the past decades, the gene expression microarray has been recognized as a feasible and useful approach to profile the molecular signatures of RCC. Recently, a breathtaking number of lncRNAs have been discovered, and altered lncRNA expression patterns have been found associated with tumorigenesis and malignancy transformation in various cancers. However, there are few lncRNAs reported in RCC. To uncover the expression pattern of lncRNAs in RCC, we investigated the lncRNA signatures of 5 RCC patients through an lncRNA microarray. To identify differentially expressed lncRNAs which may function in RCC, we evaluated the lncRNA profiles of the RCC samples relative to adjacent non-tumor tissues. We then Cryptochlorogenic-acid focused on the altered lncRNAs and validated the microarray data for two of them via qRT-PCR. There have been three previous reports of lncRNA profiles of ccRCC created through microarray. The studies of Brito et al.and Fachel et al.focused on intronic lncRNAs and revealed 6 and 29 intronic lncRNAs respectively. Furthermore, Fachel et al.identified 26 intronic lncRNAs significantly correlated with the five-year survival rates of RCC patients. However, intronic lncRNAs are only a fraction of the lncRNA Mycophenolic acid family, and other lncRNA subgroups have yet to be identified. Furthermore, not all stages of RCC have been profiled��for example, the six patients whom Yu et al.used for microarray were all at the American Joint Committee on Cancer clinical stage T1bN0M0. The samples used in the present study consisted of T1a, T1b, and T2a stages. One T1a sample had a history of radical nephrectomy because of RCCone year previously that may indicate a more aggressive malignancy. Therefore our samples cover a wider range of stages and may better reflect disorders in RCC. We also noted that few lncRNAs were deregulated in all or parts of previous studies. This may be due, at least in part, to samples taken at different stages or differences in collecting samples. In addition, the patients in these three studieswere all pathologically diagnosed with ccRCC. This may help characterize ccRCC, but does not further understanding of RCC in general or delineate the differences in disparate pathological patterns. Therefore we analyzed 70 paired tissues that comprised different patterns of RCC, including clear cell, papillary, and chromophobe carcinomas, for two lncRNAs. Primarily, we divided the samples into a ccRCC group and an nccRCC group, and we found that fold changes in the levels of AK096725 relative to non-tumoral tissues.

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