Altered expression and editing of miRNA-100 regulates iTreg differentiation

Negi, Vinny; Paul, Deepanjan; Das, Sudipta; Bajpai, Prachi; Singh, Suchita; Mukhopadhyay, Arijit; Agrawal, Anurag; Ghosh, Balaram

doi:10.1093/nar/gkv752

Cited by 47 publications

(53 citation statements)

References 30 publications

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“…The Treg cells secrete the anti-inflammatory cytokine IL-10 to attenuate inflammation. The dynamic balance between Th17 and Treg cell differentiation is mediated by regulation of cytokine, such as IL-6, IL-21, and IL-2 ( 49 , 50 ).…”

Section: The Crosstalk Between Intestinal Bacteria and Mucosal Immunementioning

confidence: 99%

Nutrients Mediate Intestinal Bacteria–Mucosal Immune Crosstalk

et al. 2018

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The intestine is the shared site of nutrient digestion, microbiota colonization and immune cell location and this geographic proximity contributes to a large extent to their interaction. The onset and development of a great many diseases, such as inflammatory bowel disease and metabolic syndrome, will be caused due to the imbalance of body immune. As competent assistants, the intestinal bacteria are also critical in disease prevention and control. Moreover, the gut commensal bacteria are essential for development and normal operation of immune system and the pathogens are also closely bound up with physiological disorders and diseases mediated by immune imbalance. Understanding how our diet and nutrient affect bacterial composition and dynamic function, and the innate and adaptive status of our immune system, represents not only a research need but also an opportunity or challenge to improve health. Herein, this review focuses on the recent discoveries about intestinal bacteria–immune crosstalk and nutritional regulation on their interplay, with an aim to provide novel insights that can aid in understanding their interactions.

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Section: The Crosstalk Between Intestinal Bacteria and Mucosal Immunementioning

confidence: 99%

Nutrients Mediate Intestinal Bacteria–Mucosal Immune Crosstalk

et al. 2018

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“…RNA editing in miRNAs has the potential to regulate the processing of precursor miRNAs into mature miRNAs (Yang et al 2006;Kawahara et al 2007a). Moreover, because miRNA regulation requires a perfect base-pairing of the seed region (2-8 position) of miRNA, a singlenucleotide change can markedly alter miRNA target recognition (Kawahara et al 2007b;Negi et al 2015). Intriguingly, several miRNA editing events appear to be critical in cancer.…”

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confidence: 99%

Systematic characterization of A-to-I RNA editing hotspots in microRNAs across human cancers

et al. 2017

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RNA editing, a widespread post-transcriptional mechanism, has emerged as a new player in cancer biology. Recent studies have reported key roles for individual miRNA editing events, but a comprehensive picture of miRNA editing in human cancers remains largely unexplored. Here, we systematically characterized the miRNA editing profiles of 8595 samples across 20 cancer types from miRNA sequencing data of The Cancer Genome Atlas and identified 19 adenosine-to-inosine (A-to-I) RNA editing hotspots. We independently validated 15 of them by perturbation experiments in several cancer cell lines. These miRNA editing events show extensive correlations with key clinical variables (e.g., tumor subtype, disease stage, and patient survival time) and other molecular drivers. Focusing on the RNA editing hotspot in miR-200b, a key tumor metastasis suppressor, we found that the miR-200b editing level correlates with patient prognosis opposite to the pattern observed for the wild-type miR-200b expression. We further experimentally showed that, in contrast to wild-type miRNA, the edited miR-200b can promote cell invasion and migration through its impaired ability to inhibit ZEB1/ZEB2 and acquired concomitant ability to repress new targets, including LIFR, a well-characterized metastasis suppressor. Our study highlights the importance of miRNA editing in gene regulation and suggests its potential as a biomarker for cancer prognosis and therapy.

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“…C-to-U RNA editing, instead, is known to be catalyzed by enzymes of the Apolipoprotein B mRNA Editing Enzyme Catalytic Polypeptide (APOBEC) family, specifically APOBEC1 and APOBEC3, at least in the context of mRNAs (Wedekind et al 2003). However, to date, no proof has been reported concerning the role of APOBECs in miRNA editing, and only a few studies have discussed this type of modification in miRNAs (Joyce et al 2011;Negi et al 2015).…”

Section: Introductionmentioning

confidence: 99%

MiREDiBase: a manually curated database of validated and putative editing events in microRNAs

Marceca

Distefano

Tomasello

et al. 2020

Preprint

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MicroRNAs (miRNAs) are a class of regulatory small non-coding RNAs that modulate gene expression. As such, miRNAs are indirectly involved in most cellular mechanisms, including cell differentiation, proliferation, survival, and homeostasis. Several different mechanisms finely regulate miRNA expression levels and functions. Among these, miRNA editing is a type of epitranscriptomic modification that alters the original nucleotide sequence of selected miRNAs, possibly influencing their conformational state and target-binding ability. To date, adenosine-to-inosine (A-to-I) and cytosine-to-uracil (C-to-U) RNA editing are recognized as the "canonical" editing types, with the A-to-I type being the predominant one. A comprehensive resource explicitly dedicated to miRNA editing data collection is still missing. Here we present MiREDiBase, a manually curated catalog of editing events in miRNAs. Overall, the current version includes 3059 unique A-to-I and C-to-U editing sites occurring in 626 human miRNA transcripts and three different species of non-human primates. Each editing event is provided with essential information and key relevant details, including biological sample, detection method, enzyme-dependent affinity, editing level, and biological function. Editing events in human mature miRNAs were provided with miRNA-target predictions and enrichment analysis. Minimum free energy structures were inferred for editing events falling into pre-miRNA regions, aiming to help users to interpret the biological information. MiREDiBase represents a valuable tool for cell biology and biomedical research, continuously updated, improved, and expanded with new data from the literature. MiREDiBase is available at https://ncrnaome.osumc.edu/miredibase.

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Altered expression and editing of miRNA-100 regulates iTreg differentiation

Cited by 47 publications

References 30 publications

Nutrients Mediate Intestinal Bacteria–Mucosal Immune Crosstalk

Nutrients Mediate Intestinal Bacteria–Mucosal Immune Crosstalk

Systematic characterization of A-to-I RNA editing hotspots in microRNAs across human cancers

MiREDiBase: a manually curated database of validated and putative editing events in microRNAs

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