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Abstract
BackgroundLong non-coding RNAs (lncRNAs) are not translated into proteins and were initially considered to be part of the ‘dark matter’ of the genome. Recently, it has been shown that lncRNAs play a role in the recruitment of chromatin modifying complexes and can influence gene expression. However, it is unknown if lncRNAs function in a similar way in cancer.ResultsHere, we show that the lncRNA ROR occupies and activates the TESC promoter by repelling the histone G9A methyltransferase and promoting the release of histone H3K9 methylation. Suppression of ROR in tumors results in silencing of TESC expression, and G9A-mediated histone H3K9 methylation in the TESC promoter is restored, which significantly reduces tumor growth and metastasis. Without ROR silencing, TESC knockdown presents consistent and significant reductions in tumor progression.ConclusionsOur results reveal a novel mechanism by which ROR may serve as a decoy oncoRNA that blocks binding surfaces, preventing the recruitment of histone modifying enzymes, thereby specifying a new pattern of histone modifications that promote tumorigenesis.Electronic supplementary materialThe online version of this article (doi:10.1186/s13059-015-0705-2) contains supplementary material, which is available to authorized users.
Highlights
Long non-coding RNAs are not translated into proteins and were initially considered to be part of the ‘dark matter’ of the genome
Only a small number of functional Long non-coding RNAs (lncRNAs) have been well characterized to date, these lncRNAs have been shown to control every level of the gene expression program [7], and a series of studies have further revealed that lncRNAs accomplish their functional roles
We demonstrate that ROR lncRNA acts as a necessary decoy oncoRNA that plays an important regulatory role in tumorigenesis and represents a novel style of histone modification
Summary
Long non-coding RNAs (lncRNAs) are not translated into proteins and were initially considered to be part of the ‘dark matter’ of the genome. It has been shown that lncRNAs play a role in the recruitment of chromatin modifying complexes and can influence gene expression. It is unknown if lncRNAs function in a similar way in cancer. Only a small number of functional lncRNAs have been well characterized to date, these lncRNAs have been shown to control every level of the gene expression program [7], and a series of studies have further revealed that lncRNAs accomplish their functional roles. Human LncRNA ROR, at only 2.6 kb in length, has been shown to reprogram differentiated cells to induced pluripotent stem cells (iPSCs) by directly targeted
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