Expression of miRNAs miR-133b and miR-206 in the Il17a/f Locus Is Co-Regulated with IL-17 Production in αβ and γδ T Cells

Haas, Julian; Nistala, Kiran; Petermann, Franziska; Saran, Namita; Chennupati, Vijaykumar; Schmitz, Susanne; Korn, Thomas; Wedderburn, Lucy R.; Förster, Reinhold; Krueger, Andreas; Prinz, Immo

doi:10.1371/journal.pone.0020171

Cited by 53 publications

(51 citation statements)

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“…miR-133b, located on chromosome 6p12.2, has been studied in midbrain dopamine neurons [17], cardiomyocytes [18], skeletal muscles [19], extraocular muscles [20], myoblasts [21], osteoblasts [22], T-helper cells [23], and coronary artery disease [24]. More recently, miR-133b has been suggested to function as a tumor suppressor gene, because it was shown to be downregulated in several cancer types as compared with normal tissues, including lung cancer [25], esophageal squamous cell carcinoma [26], colorectal cancer [27], gastric cancer [28], bladder cancer [29], squamous cell carcinoma of the tongue [30], cervical carcinoma [31], breast cancer, lymphoma, ovarian cancer, prostate cancer, and testicular cancer [32].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐133b inhibits the growth of non‐small‐cell lung cancer by targeting the epidermal growth factor receptor

et al. 2012

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Both the deregulation of microRNAs and epidermal growth factor receptor (EGFR) are emerging as important factors in non‐small‐cell lung cancer (NSCLC). Here, miR‐133b was found to be associated with tumor stage, the extent of regional lymph node involvement, stage, visceral pleura or vessel invasion and EGFR mRNA expression in Chinese patients with NSCLC. Bioinformatic analysis and luciferase reporter assay revealed that miR‐133b can interact specifically with the 3′‐UTR of EGFR mRNA. Functionally, miR‐133b transfection showed regulatory activity in translationally repressing EGFR mRNA. Moreover, miR‐133b transfection may modulate apoptosis, invasion and sensitivity to EGFR‐TKI through the EGFR signaling pathways, especially in EGFR‐addicted NSCLC cells. Taken together, our findings show that miR‐133b can inhibit cell growth of NSCLC through targeting EGFR and regulating its downstream signaling pathway. This finding has important implications for the development of targeted therapeutics for a number of EGFR‐addicted cancers.

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Section: Discussionmentioning

confidence: 99%

MicroRNA‐133b inhibits the growth of non‐small‐cell lung cancer by targeting the epidermal growth factor receptor

et al. 2012

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“…MiR133b and 206 have been previously reported to be expressed during differentiation of im munocompetent mouse Th17 cells, with miR133b/206 cistron transcription occurring along with expression at the nearby Il17a/f gene locus [80] . This feature of T cell differentiation towards an IL17producing phenotype is shared between αβ and γδ T cells, where the specific coregulation of miR133b and miR206 with the Il17a/f locus extends to human Th17 cells, suggesting presence of miR-133b/-206 in T cells may be biomarkers for Th17-type immunoreactions.…”

Section: Responsesmentioning

confidence: 99%

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Mitchelson¹

2015

WJBC

140

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MicroRNAs are small non-coding RNAs that participate in different biological processes, providing subtle combinational regulation of cellular pathways, often by regulating components of signalling pathways. Aberrant expression of miRNAs is an important factor in the development and progression of disease. The canonical myomiRs (miR-1, -133 and -206) are central to the development and health of mammalian skeletal and cardiac muscles, but new findings show they have regulatory roles in the development of other mammalian non-muscle tissues, including nerve, brain structures, adipose and some specialised immunological cells. Moreover, the deregulation of myomiR expression is associated with a variety of different cancers, where typically they have tumor suppressor functions, although examples of an oncogenic role illustrate their diverse function in different cell environments. This review examines the involvement of the related myomiRs at the crossroads between cell development/ tissue regeneration/tissue inflammation responses, and cancer development. Core tip: The roles of the canonical muscle-associated microRNAs are reviewed, including microRNA families miR-1 and miR-133, and single miR-206, which are collectively known as the "myomiRs". The myomiRs act at the crossroads of the molecular regulation of muscle cells, linking between pathways for cell differentiation, development and maintenance, but also potentiate aberrant cell growth in numerous non-muscle cancers. Typically myomiRs are downregulated in cancers, but some myomiRs are upregulated in a few cancers, yet each dysregulation event advances tumor progression. The review examines normal and disease-linked molecular changes associated with the myomiRs, and collates the extensive literature into accessible tables. REVIEW

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“…+ T cells to differentiate to IL-17-producing cells or other Th lineages [32]. Finally, a most interesting example of cytokine/miRNA crossregulation comes from IFN-γ and miR-29.…”

Section: Cytokine-mediated Regulation Of Mirna Expression On T Cellsmentioning

confidence: 99%

“…For example, the expression of the miR-133b/miR-206 cluster, which lies in proximity to, and is coexpressed with, the Il17a/f locus in IL-17-producing αβ and γδ T cells [32], is specifically induced by IL-23, whereas other "Th17-polarizing" cytokines, such as IL-6, TGF-β, or IL-1β, have minimal effects on miR-133b/miR-206 expression [32]. The significance of this phenomenon is still unknown since forced overexpression of the miR-133b/miR-206 cluster in vitro and in vivo had minimal effect on the potential of naïve CD4+ T cells to differentiate to IL-17-producing cells or other Th lineages [32]. Finally, a most interesting example of cytokine/miRNA crossregulation comes from IFN-γ and miR-29.…”

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confidence: 99%

Cross‐regulation between cytokine and microRNA pathways in T cells

et al. 2015

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microRNA (miRNA) mediated regulation of protein expression has emerged as an important mechanism in T-cell physiology, from development and survival to activation, proliferation, and differentiation. One of the major classes of proteins involved in these processes are cytokines, which are both key input signals and major products of T-cell function. Here, we summarize the current data on the molecular cross-talk between cytokines and miRNAs: how cytokines regulate miRNA expression, and how specific miRNAs control cytokine production in T cells. We also describe the inflammatory consequences of deregulating the miRNA/cytokine axis in mice and humans. We believe this topical area will have key implications for immune modulation and treatment of autoimmune pathology. Keywords:Cytokines r Inflammation r miRNA r T cells microRNAs as regulators of protein expressionBiological processes require the integration of environmental stimuli at the level of gene expression. The robustness of genetic networks depends on the distinction between physiological responses (to particular cues) and biological "noise" (stochastic variations), which can be achieved, for example, by establishing feed-forward transcriptional loops. Over the past two decades, a new mechanism that interacts with transcriptional loops and sets additional thresholds, which enable cells to filter physiological signals from noise has emerged; this mechanism regulates gene expression at the posttranscriptional level and relies on microRNAs (miRNAs; reviewed in [1]). These are an abundant class of evolutionarily conserved small noncoding (untranslated) RNA species that control target mRNA stability, degradation, and translation, thus affecting the majority of mammalian genes [2].Correspondence: Dr. Anita Q. Gomes e-mail: anitagomes@medicina.ulisboa.ptIn the conventional miRNA biogenesis pathway, RNA polymerase II transcribed pri-miRNAs are processed by the nuclear RNase III enzyme Drosha (complexed with DGCR8) to generate 60-70 nt stem-loop intermediates, the pre-miRNAs, that are further processed into 19-24mers in the cytoplasm by another key RNase III, Dicer. Mature miRNAs are then incorporated into RNAinduced silencing complexes, whose core components are proteins of the Argonaute family (Ago1-4), which use the 5 end (nucleotides 2-8) "seed sequence" of the miRNA to recognize complementary mRNA transcripts (mostly in their 3 untranslated region) for deadenylation or inhibition of translation, ultimately resulting in mRNA decapping and decay (reviewed in [3,4]).Unique spatial and temporal expression patterns in distinct hematopoietic cell lineages are suggestive of multiple roles for miRNAs in hematopoiesis, self-tolerance, and in immune responses, which have been explored over the past decade (reviewed in [5,6]). Over a 100 different miRNAs have been shown to be expressed by cells of the immune system, where * These authors contributed equally to this work as first authors. * * These authors contributed equally to this work as last authors.C 2015 WILEY-VCH Ve...

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Expression of miRNAs miR-133b and miR-206 in the Il17a/f Locus Is Co-Regulated with IL-17 Production in αβ and γδ T Cells

Cited by 53 publications

References 49 publications

MicroRNA‐133b inhibits the growth of non‐small‐cell lung cancer by targeting the epidermal growth factor receptor

MicroRNA‐133b inhibits the growth of non‐small‐cell lung cancer by targeting the epidermal growth factor receptor

Roles of the canonical myomiRs miR-1, -133 and -206 in cell development and disease

Cross‐regulation between cytokine and microRNA pathways in T cells

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