Abstract
MicroRNAs (miRNAs) are highly conserved elements in mammals, and exert key regulatory functions. Growing evidence shows that miRNAs can interact with another class of non-coding RNAs, so-called transcribed ultraconserved regions (T-UCRs), which take part in transcriptional, post-transcriptional and epigenetic regulation processes. We report here the interaction of miRNAs and T-UCRs as a network modulating the availability of these non-coding RNAs in bladder cancer cells. In our cell system, antagomiR-596 increased the expression of T-UCR 201+. Moreover, T-UCR 8+ silencing increased miR-596 expression, which in turn reduced total T-UCR 283+, showing that the perturbation of one element in this network changes the expression of other interactors. In addition, we identify the polycomb protein Yin Yang 1 (YY1) as mediator of binding between miR-596 and T-UCR 8+. These new findings describe for the first time a network between T-UCRs, miRNAs and YY1 protein, highlighting the existence of an additional layer of gene expression regulation.
Highlights
We focused on the 293 transcribed ultraconserved regions (T-UCRs) (≈ 60% of all T-UCRs analysed) that were differentially expressed at a statistically significant level (p < 0.05, q < 0.025) in bladder cancer (BlCa) tissues
Differential expression of Transcribed ultraconserved ultraconserved regions (T‐UCRs) has been reported in BlCa tissues, the mechanism remains unknown
We have computationally identified a network of nine T-UCRs (T-UCR 8+, that share binding sites for miR‐596. miR‐596 is located at the short arm of chromosome 8, which is 195+, 201+, 283+, 305+, 388+, 390+, 393+ and 457+), both up- and downregulated in BlCa tissues that often affected by focal break points in cancer [45]
Summary
Long non-coding RNAs (lncRNAs) have been shown to play crucial roles in a variety of biological processes such as epigenetic control of gene expression, promoter-specific gene regulation [1,2,3], X-chromosome inactivation [4,5,6], imprinting [7,8,9,10,11], and maintenance of nuclear architecture [12,13,14] They have been implicated in many different diseases including cancer [15,16]. Recent data suggest that T-UCRs are preferentially located in the cytoplasm, where they are able to establish interactions with other transcripts [21]
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