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Assessing the ceRNA hypothesis with quantitative measurements of miRNA and target abundance

GSE52801 Mus musculus Expression profiling by high throughput sequencing; Non-coding RNA profiling by high throughput sequencing 33 samples Submitted 2014/05/01 Platform GPL13112
Summary
Recent studies have reported that competitive endogenous RNAs (ceRNAs) can act as sponges for a miRNA through their binding sites and that changes in ceRNA abundances from individual genes can modulate the miRNA’s activity. Consideration of this hypothesis would benefit from knowing the quantitative relationship between a miRNA and its endogenous target sites. Here, we altered intracellular target-site abundance through expression of a miR-122 target in hepatocytes and livers, and analyzed the effects on miR-122 target genes. Target repression was released in a threshold-like manner at high target-site abundance (≥1.5x10^5 added target sites per cell), and this threshold was insensitive to the effective levels of the miRNA. Furthermore, in response to extreme metabolic liver disease models, global target-site abundance of hepatocytes did not change sufficiently to affect miRNA-mediated repression. Thus, modulation of miRNA target abundance is unlikely to cause significant effects on gene expression and metabolism through a ceRNA effect.
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Direct links to NCBI, no account and no request form: the whole study as GSE52801_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 33 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA230067 and SRA study SRP033367. Searching any of these in the dataset finder brings you back here.

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