RNAa in action: From the exception to the norm

Guo, Dan; Barry, Liam P.; Lin, Sharon Szu Hua; Huang, Vera; Li, Long-Cheng

doi:10.4161/15476286.2014.972853

Cited by 28 publications

(18 citation statements)

References 34 publications

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“…Finally, the ability of mammalian RNAi factors to be present and functional in cell nuclei has been open to debate. Recent evidence, however, has shown that RNAi factors exist in mammalian nuclei 26 34 35 36 37 38 39 40 and can be active controlling splicing 37 41 or transcription 24 25 42 43 44 . Our results widen the reach of nuclear RNAi by suggesting that it can be used to target intronic RNA, interfere with R-loop formation, and release the break on transcription.…”

Section: Discussionmentioning

confidence: 99%

Activating frataxin expression by repeat-targeted nucleic acids

Matsui

Corey

2016

Nat Commun

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Friedreich's ataxia is an incurable genetic disorder caused by a mutant expansion of the trinucleotide GAA within an intronic FXN RNA. This expansion leads to reduced expression of frataxin (FXN) protein and evidence suggests that transcriptional repression is caused by an R-loop that forms between the expanded repeat RNA and complementary genomic DNA. Synthetic agents that increase levels of FXN protein might alleviate the disease. We demonstrate that introducing anti-GAA duplex RNAs or single-stranded locked nucleic acids into patient-derived cells increases FXN protein expression to levels similar to analogous wild-type cells. Our data are significant because synthetic nucleic acids that target GAA repeats can be lead compounds for restoring curative FXN levels. More broadly, our results demonstrate that interfering with R-loop formation can trigger gene activation and reveal a new strategy for upregulating gene expression.

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Section: Discussionmentioning

confidence: 99%

Activating frataxin expression by repeat-targeted nucleic acids

Matsui

Corey

2016

Nat Commun

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“…The most discussed modus operandi of miRs is post-transcriptional gene silencing, however miRs are also known to perform functions such as activation of transcription. There are several examples in the literature that describe this contrary role of miRs on gene transcription by targeting promoter elements, a phenomenon known as RNA activation (RNAa) [102,103]. Matsui et al reported the existence of RNA transcripts that have MRE for an endogenous miR-589 and overlap the cyclooxygenase-2 (COX-2) promoter.…”

Section: Non-canonical Mirs In the Tmementioning

confidence: 99%

MicroRNAs as Emerging Regulators of Signaling in the Tumor Microenvironment

Syed

Brüne

2020

Cancers

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A myriad of signaling molecules in a heuristic network of the tumor microenvironment (TME) pose a challenge and an opportunity for novel therapeutic target identification in human cancers. MicroRNAs (miRs), due to their ability to affect signaling pathways at various levels, take a prominent space in the quest of novel cancer therapeutics. The role of miRs in cancer initiation, progression, as well as in chemoresistance, is being increasingly investigated. The canonical function of miRs is to target mRNAs for post-transcriptional gene silencing, which has a great implication in first-order regulation of signaling pathways. However, several reports suggest that miRs also perform non-canonical functions, partly due to their characteristic non-coding small RNA nature. Examples emerge when they act as ligands for toll-like receptors or perform second-order functions, e.g., to regulate protein translation and interactions. This review is a compendium of recent advancements in understanding the role of miRs in cancer signaling and focuses on the role of miRs as novel regulators of the signaling pathway in the TME.

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“…Thus, since PIWI is required for the expression of this reporter gene in a dose-dependent manner, it is shown to promote the active epigenetic state of 3R-TAS [ 35 ]. Additionally, in Caenorhabditis elegans , the piRNA and Argonaute protein CSR-1 complex has been shown to cause additional recruitment of histone modifying enzymes, which result in epigenetic activation [ 57 ].…”

Section: The Pirna/piwi Protein Interaction In Germline and Somatic Tmentioning

confidence: 99%

Piwi-interacting RNAs in cancer: emerging functions and clinical utility

et al. 2016

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PIWI-interacting RNAs (piRNAs) are emerging players in cancer genomics. Originally described in the germline, there are over 20,000 piRNA genes in the human genome. In contrast to microRNAs, piRNAs interact with PIWI proteins, another member of the Argonaute family, and function primarily in the nucleus. There, they are involved in the epigenetic silencing of transposable elements in addition to the transcriptional regulation of genes. It has recently been demonstrated that piRNAs are also expressed across a variety of human somatic tissue types in a tissue-specific manner. An increasing number of studies have shown that aberrant piRNA expression is a signature feature across multiple tumour types; however, their specific tumorigenic functions remain unclear. In this article, we discuss the emerging functional roles of piRNAs in a variety of cancers, and highlight their potential clinical utilities.

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RNAa in action: From the exception to the norm

Cited by 28 publications

References 34 publications

Activating frataxin expression by repeat-targeted nucleic acids

Activating frataxin expression by repeat-targeted nucleic acids

MicroRNAs as Emerging Regulators of Signaling in the Tumor Microenvironment

Piwi-interacting RNAs in cancer: emerging functions and clinical utility

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