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Non-Coding RNA, Volume 1, Issue 3 (December 2015) – 6 articles , Pages 170-288

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632 KiB

Open AccessEditorial

The Non-Coding RNA Journal Club: Highlights on Recent Papers—3

by Ioana Berindan-Neagoe, George Adrian Calin, Claire Francastel, Florent Hubé and Gaetano Santulli

Non-Coding RNA 2015, 1(3), 285-288; https://doi.org/10.3390/ncrna1030285 - 21 Dec 2015

Cited by 1 | Viewed by 4511

Abstract

We are glad to share with you our third Journal Club and to highlight some of the most interesting papers published recently. [...] Full article

(This article belongs to the Collection The Non-Coding RNA Journal Club: Highlights on Recent Papers)

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Open AccessArticle

Truncated Isoforms of lncRNA ANRIL Are Overexpressed in Bladder Cancer, But Do Not Contribute to Repression of INK4 Tumor Suppressors

by Michèle J. Hoffmann, Judith Dehn, Johanna Droop, Günter Niegisch, Christian Niedworok, Tibor Szarvas and Wolfgang A. Schulz

Non-Coding RNA 2015, 1(3), 266-284; https://doi.org/10.3390/ncrna1030266 - 17 Dec 2015

Cited by 22 | Viewed by 6532

Abstract

The INK4/ARF locus at chromosome 9p21 encoding p14^ARF, p15^INK4B and p16^INK4A is a major tumor suppressor locus, constituting an important barrier for tumor growth. It is frequently inactivated in cancers, especially in urothelial carcinoma (UC). In addition to deletions and DNA hypermethylation, further epigenetic mechanisms might underlie its repression. One candidate factor is the long noncoding RNA ANRIL, which recruits Polycomb proteins (PcG) to regulate expression of target genes in cis and trans. We observed ANRIL overexpression in many UC tissues and cell lines mainly resulting from upregulation of 3’-truncated isoforms. However, aberrant ANRIL expression was neither associated with repression of INK4/ARF genes nor with proliferation activity or senescence. We wondered whether truncated ANRIL isoforms exhibit altered properties resulting in loss of function in cis. We excluded delocalization and performed RNA immunoprecipitation demonstrating interaction between full length or truncated ANRIL and PcG protein CBX7, but not SUZ12 of PRC2. Our data indicate that ANRIL in UC cells may not interact with PRC2, which is central for initializing gene repression. Thus, tissue-specific binding activities between ANRIL and PcG proteins may determine the regulatory function of ANRIL. In conclusion, ANRIL does not play a major role in repression of the INK4/ARF locus in UC. Full article

(This article belongs to the Section Long Non-Coding RNA)

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1019 KiB

Open AccessArticle

Antisense Activity across the Nesp Promoter is Required for Nespas-Mediated Silencing in the Imprinted Gnas Cluster

by Charlotte J. Tibbit, Christine M. Williamson, Stuti Mehta, Simon T. Ball, Mita Chotalia, Wade T. Nottingham, Sally A. Eaton, Mohamed M. Quwailid, Lydia Teboul, Gavin Kelsey and Jo Peters

Non-Coding RNA 2015, 1(3), 246-265; https://doi.org/10.3390/ncrna1030246 - 30 Nov 2015

Cited by 10 | Viewed by 5868

Abstract

Macro long non-coding RNAs (lncRNAs) play major roles in gene silencing in inprinted gene clusters. Within the imprinted Gnas cluster, the paternally expressed Nespas lncRNA downregulates its sense counterpart Nesp. To explore the mechanism of action of Nespas, we generated two new knock-in alleles to truncate Nespas upstream and downstream of the Nesp promoter. We show that Nespas is essential for methylation of the Nesp differentially methylated region (DMR), but higher levels of Nespas are required for methylation than are needed for downregulation of Nesp. Although Nespas is transcribed for over 27 kb, only Nespas transcript/transcription across a 2.6 kb region that includes the Nesp promoter is necessary for methylation of the Nesp DMR. In both mutants, the levels of Nespas were extraordinarily high, due at least in part to increased stability, an effect not seen with other imprinted lncRNAs. However, even when levels were greatly raised, Nespas remained exclusively cis-acting. We propose Nespas regulates Nesp methylation and expression to ensure appropriate levels of expression of the protein coding transcripts Gnasxl and Gnas on the paternal chromosome. Thus, Nespas mediates paternal gene expression over the entire Gnas cluster via a single gene, Nesp. Full article

(This article belongs to the Section Long Non-Coding RNA)

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1171 KiB

Open AccessArticle

miRNA–mRNA Conflux Regulating Immunity and Oxidative Stress Pathways in the Midgut of Blood-Fed Anopheles stephensi

by Shanu Jain, Jatin Shrinet, Adak Tridibes, Raj K. Bhatnagar and Sujatha Sunil

Non-Coding RNA 2015, 1(3), 222-245; https://doi.org/10.3390/ncrna1030222 - 19 Nov 2015

Cited by 4 | Viewed by 6550

Abstract

Blood feeding in Anopheles stephensi initiates a cascade of events that modulate several physiological functions in the mosquito. The midgut epithelium activates several of its molecules, most important among these being microRNAs, which regulate some of the physiological changes by targeting diverse mRNAs. The present study was conducted to identify and evaluate interactions between targets of eight miRNAs that are regulated on blood feeding. Identified from our previous study, we show these eight miRNAs exhibited distinct tissue specific expression. Targets of these miRNAs were predicted using computational approaches involving bioinformatics, co-expression analysis of the transcriptome and miRNome of blood-fed An. stephensi midgut. Using degradome sequencing, we identified some cleaved mRNAs of these microRNAs and, by using antagomiR knockdown technology to repress the miRNAs, the targets were validated in an An. stephensi cell line and in An. stephensi mosquitoes. In-depth analysis of predicted and identified targets revealed that the regulated miRNAs modulate well-characterized molecules that are involved in combating oxidative stress and immunity pathways through a dynamic miRNA:mRNA network. Our study is the first to identify miRNA:mRNA interactomes that play important role in maintaining redox homeostasis during blood feeding in the midgut of An. stephensi. Full article

(This article belongs to the Section Small Non-Coding RNA)

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Open AccessReview

The Role of MicroRNAs in Kidney Disease

by Sydwell Mukhadi, Rodney Hull, Zukile Mbita and Zodwa Dlamini

Non-Coding RNA 2015, 1(3), 192-221; https://doi.org/10.3390/ncrna1030192 - 18 Nov 2015

Cited by 25 | Viewed by 9943

Abstract

MicroRNAs (miRNAs) are short noncoding RNAs that regulate pathophysiological processes that suppress gene expression by binding to messenger RNAs. These biomolecules can be used to study gene regulation and protein expression, which will allow better understanding of many biological processes such as cell cycle progression and apoptosis that control the fate of cells. Several pathways have also been implicated to be involved in kidney diseases such as Transforming Growth Factor-β, Mitogen-Activated Protein Kinase signaling, and Wnt signaling pathways. The discovery of miRNAs has provided new insights into kidney pathologies and may provide new innovative and effective therapeutic strategies. Research has demonstrated the role of miRNAs in a variety of kidney diseases including renal cell carcinoma, diabetic nephropathy, nephritic syndrome, renal fibrosis, lupus nephritis and acute pyelonephritis. MiRNAs are implicated as playing a role in these diseases due to their role in apoptosis, cell proliferation, differentiation and development. As miRNAs have been detected in a stable condition in different biological fluids, they have the potential to be tools to study the pathogenesis of human diseases with a great potential to be used in disease prognosis and diagnosis. The purpose of this review is to examine the role of miRNA in kidney disease. Full article

(This article belongs to the Section Small Non-Coding RNA)

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Open AccessArticle

Epstein-Barr Virus EBER Transcripts Affect miRNA-Mediated Regulation of Specific Targets and Are Processed to Small RNA Species

by Julia Alles, Daniele Hasler, Syed Mohammad Ali Kazmi, Mathias Tesson, Andrew Hamilton, Linda Schlegel, Stefanie Marx, Norbert Eichner, Richard Reinhardt, Gunter Meister, Joanna B. Wilson and Friedrich A. Grässer

Non-Coding RNA 2015, 1(3), 170-191; https://doi.org/10.3390/ncrna1030170 - 30 Sep 2015

Cited by 7 | Viewed by 7683

Abstract

The oncogenic Epstein-Barr virus (EBV) expresses 44 mature microRNAs and two non-coding EBER RNAs of 167 (EBER1) and 172 (EBER2) nt length. MiRNA profiling of NK/T cell lines and primary cells and Northern blotting of EBV-infected cell lines and primary tumors revealed processing of EBER1 to short 5′-derived RNAs of approximately 23, 52 and 70 nt (EBER123, EBER152, and EBER170) and of EBER2 to 3′ fragments. The biogenesis of these species is independent of Dicer, and EBER123 does not act like a miRNA OPEN ACCESS Non-Coding RNA 2015, 1 171 to target its complementary sequence. EBER1, EBER2 and EBER123 were bound by the lupus antigen (La), a nuclear and cytoplasmic protein that facilitates RNAi. Consistent with this, the EBERs affect regulation of interleukin 1alpha (IL1α) and RAC1 reporters harboring miR target sequences, targets of miR-142-3p. However, the EBERs have no effect upon another target of miR-142-3p, ADCY9, nor on TOMM22, a target of ebv-miR-BART16, indicative of selective modulation of gene expression by the EBERs. Full article

(This article belongs to the Section Small Non-Coding RNA)

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