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MiR-26 dampens IL-6 production by down-regulating TNF-a/NF-kB signaling through silencing HMGA1 and MALT1 and not by directly targeting IL-6 mRNA

ABSTRACT: We found NF-kB signaling as a major target of miR-26 based on an analysis of the changes in gene activation by TNF-a in response to alteration of miR-26 levels.

ORGANISM(S): Homo sapiens

PROVIDER: GSE70831 | GEO | 2016/03/31

SECONDARY ACCESSION(S): PRJNA289656

REPOSITORIES: GEO

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MiR-26 dampens IL-6 production by down-regulating TNF-a/NF-kB signaling through silencing HMGA1 and MALT1 and not by directly targeting IL-6 mRNA

Project description:We found NF-kB signaling as a major target of miR-26 based on an analysis of the changes in gene activation by TNF-a in response to alteration of miR-26 levels. Transcriptional profiling of genes in response to either a miR-26 mimic or miR-26 antagomir.

2016-03-31 | E-GEOD-70831 | biostudies-arrayexpress

MiR-26 down-regulates TNF-α/NF-κB signalling and IL-6 expression by silencing HMGA1 and MALT1.

Project description:MiR-26 has emerged as a key tumour suppressor in various cancers. Accumulating evidence supports that miR-26 regulates inflammation and tumourigenicity largely through down-regulating IL-6 production, but the underlying mechanism remains obscure. Here, combining a transcriptome-wide approach with manipulation of cellular miR-26 levels, we showed that instead of directly targeting IL-6 mRNA for gene silencing, miR-26 diminishes IL-6 transcription activated by TNF-α through silencing NF-κB signalling related factors HMGA1 and MALT1. We demonstrated that miR-26 extensively dampens the induction of many inflammation-related cytokine, chemokine and tissue-remodelling genes that are activated via NF-κB signalling pathway. Knocking down both HMGA1 and MALT1 by RNAi had a silencing effect on NF-κB-responsive genes similar to that caused by miR-26. Moreover, we discovered that poor patient prognosis in human lung adenocarcinoma is associated with low miR-26 and high HMGA1 or MALT1 levels and not with levels of any of them individually. These new findings not only unravel a novel mechanism by which miR-26 dampens IL-6 production transcriptionally but also demonstrate a direct role of miR-26 in down-regulating NF-κB signalling pathway, thereby revealing a more critical and broader role of miR-26 in inflammation and cancer than previously realized.

| S-EPMC4856999 | biostudies-literature

The miR-26 family regulates neural differentiation-associated microRNAs and mRNAs by directly targeting REST

Project description:Our data identify the miR-26 family as a trigger of a self-amplifying system essential for neural differentiation that acts upstream REST-controlled miRs and initiate a neuronal gene expression program.

2021-04-09 | GSE171727 | GEO

miR-26 suppresses adipocyte progenitor differentiation and fat production by targeting Fbxl19

Project description:Purpose: Fat storage in adult mammals is a highly regulated process that involves the mobilization of adipocyte progenitor cells (APCs) that differentiate to produce new adipocytes. Here we report an unexpected role for the broadly conserved miR-26 family of microRNAs (miR-26a-1, miR-26a-2, and miR-26b) as key regulators of APC differentiation. Global loss of miR-26 resulted in a dramatic expansion of adipose tissue in adult mice fed normal chow. Conversely, transgenic overexpression of miR-26a protected mice from high fat diet-induced obesity. These effects were attributable to a cell-autonomous function of miR-26 as a potent inhibitor of APC differentiation. miR-26 blocks adipogenesis, at least in part, by repressing expression of Fbxl19, a conserved miR-26 target without a previously known role in adipocyte biology that encodes a component of SCF-type E3 ubiquitin ligase complexes. These findings have therefore revealed a new pathway that plays a critical role in regulating adipose tissue formation in vivo and suggest new potential therapeutic targets for obesity and related disorders.

2020-01-21 | GSE134736 | GEO

Adult onset cataract formation following loss of miR-26 results from deregulated inflammation and loss of epithelial homeostasis

Project description:Despite strong evidence that normal lens development and function requires regulation governed by miRNAs, the role of specific miRNAs in mammalian lens FEV development and homeostasis remains largely unexplored. Here we undertook a comprehensive RNA-seq analysis of miRNA transcripts in the newborn mouse lens, exploring both differential expression between lens epithelial cells and lens fiber cells and overall miRNA abundance. We then selected the three most abundant lens miRNAs: miR-184, miR-1 and miR-26 for functional analysis. Of these three miRNAs, only miR-1, which was highly expressed in lens fiber cells, exhibited significant differential expression. Mouse lenses lacking miR-184, or both copies of miR-1, or all three copies of miR-26 exhibited morphologically normal prenatal lens development. However, mice lacking all three copies of miR-26 (miR-26KO) developed postnatal cataracts at approximately 4-6 weeks of age. RNA-seq analysis of neonatal lenses from miR-26KO mice demonstrated a deregulation of the complement pathway, inflammation and epithelial to mesenchymal transition

2024-05-08 | GSE252611 | GEO

Tumor suppression by miR-26 overrides potential oncogenic activity in intestinal tumorigenesis

Project description:Through a series of mouse genetic studies, we concluded that miR-26 overexpression in intestinal epithelial cells inhibits tumor formation in Apcmin/+ mice. We isolated intestinal epithelial cells from M2rtTA and M2rtTA; eGFP.miR-26a to assess gene expression changes after the induction of miR-26a expression.

2014-10-30 | GSE62831 | GEO

Malt1 protease inactivation efficiently dampens immune responses but causes spontaneous autoimmunity.

Project description:The protease activity of the paracaspase Malt1 has recently gained interest as a drug target for immunomodulation and the treatment of diffuse large B-cell lymphomas. To address the consequences of Malt1 protease inactivation on the immune response in vivo, we generated knock-in mice expressing a catalytically inactive C472A mutant of Malt1 that conserves its scaffold function. Like Malt1-deficient mice, knock-in mice had strong defects in the activation of lymphocytes, NK and dendritic cells, and the development of B1 and marginal zone B cells and were completely protected against the induction of autoimmune encephalomyelitis. Malt1 inactivation also protected the mice from experimental induction of colitis. However, Malt1 knock-in mice but not Malt1-deficient mice spontaneously developed signs of autoimmune gastritis that correlated with an absence of Treg cells, an accumulation of T cells with an activated phenotype and high serum levels of IgE and IgG1. Thus, removal of the enzymatic activity of Malt1 efficiently dampens the immune response, but favors autoimmunity through impaired Treg development, which could be relevant for therapeutic Malt1-targeting strategies.

| S-EPMC4282555 | biostudies-literature

Transcriptomics of THP-1 macrophages treated with or without IL-26 for 24h

Project description:Purpose: The aim of this study was to obtain a comprehensive transcriptomic analysis of IL-26-exposed macrophages. Methods: THP-1 derived macrophage were generated by incubating THP-1 cells with PMA (50 ng/ml) for 24h.Then THP-1 macrophages were treated with IL-26 for 24h, which were collected and applied to RNA-sequencing. The constructed sequencing library was sequenced using an Illumina Novaseq 6000 system. The expression of transcripts was calculated as fragments per kilobase of exon model per million mapped reads (FPKM). Results: In total, we identified 1303 differentially expressed protein-coding genes between untreated and IL-26-treated macrophages, including 667 up-regulated and 636 down-regulated genes.

2022-04-27 | GSE192493 | GEO

Comamonas sp. 26 strain:26

Project description:Comamonas sp. 26 strain:26 Genome sequencing and assembly

| PRJNA402406 | ENA

CLIP libraries for SUP-26::FLAG

Project description:Gene expression in early animal embryogenesis is in large part controlled post-transcriptionally. Maternally-contributed microRNAs may therefore play important roles in early development. We have elucidated a major biological role of the nematode mir-35 family of maternally-contributed, essential microRNAs. We show that this microRNA family regulates the sex determination pathway at multiple levels, acting both upstream and downstream of her-1 to prevent aberrantly activated male developmental programs in hermaphrodite embryos. The predicted target genes that act downstream of the mir-35 family in this process, sup-26 and nhl-2, both encode RNA binding proteins, thus delineating a previously unknown post-transcriptional regulatory subnetwork within the well-studied sex determination pathway of C. elegans. Repression of nhl-2 by the mir-35 family is not only required for proper sex determination but also for viability, showing that a single microRNA target site can be essential. Since sex determination in C. elegans requires zygotic gene expression to read the sex chromosome karyotype, early embryos must remain gender-naïve; our findings show that the mir-35 family microRNAs act in the early embryo to function as a developmental timer that preserves naïveté and prevents premature deleterious developmental decisions.

2017-02-10 | GSE94703 | GEO

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