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Non-Coding RNA, Volume 3, Issue 3 (September 2017)

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Research

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Open AccessArticle Rare Splice Variants in Long Non-Coding RNAs
Non-Coding RNA 2017, 3(3), 23; doi:10.3390/ncrna3030023
Received: 18 May 2017 / Revised: 24 June 2017 / Accepted: 29 June 2017 / Published: 5 July 2017
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Abstract
Long non-coding RNAs (lncRNAs) form a substantial component of the transcriptome and are involved in a wide variety of regulatory mechanisms. Compared to protein-coding genes, they are often expressed at low levels and are restricted to a narrow range of cell types or
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Long non-coding RNAs (lncRNAs) form a substantial component of the transcriptome and are involved in a wide variety of regulatory mechanisms. Compared to protein-coding genes, they are often expressed at low levels and are restricted to a narrow range of cell types or developmental stages. As a consequence, the diversity of their isoforms is still far from being recorded and catalogued in its entirety, and the debate is ongoing about what fraction of non-coding RNAs truly conveys biological function rather than being “junk”. Here, using a collection of more than 100 transcriptomes from related B cell lymphoma, we show that lncRNA loci produce a very defined set of splice variants. While some of them are so rare that they become recognizable only in the superposition of dozens or hundreds of transcriptome datasets and not infrequently include introns or exons that have not been included in available genome annotation data, there is still a very limited number of processing products for any given locus. The combined depth of our sequencing data is large enough to effectively exhaust the isoform diversity: the overwhelming majority of splice junctions that are observed at all are represented by multiple junction-spanning reads. We conclude that the human transcriptome produces virtually no background of RNAs that are processed at effectively random positions, but is—under normal circumstances—confined to a well defined set of splice variants. Full article
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Open AccessCommunication Expression Profiling Identifies the Noncoding Processed Transcript of HNRNPU with Proliferative Properties in Pancreatic Ductal Adenocarcinoma
Non-Coding RNA 2017, 3(3), 24; doi:10.3390/ncrna3030024
Received: 21 July 2017 / Revised: 10 August 2017 / Accepted: 21 August 2017 / Published: 25 August 2017
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Abstract
A gene array was used to profile the expression of 22,875 long non-coding RNAs (lncRNAs) and a large number of protein coding genes in 47 specimens of pancreatic ductal adenocarcinoma (PDAC), adjacent benign pancreas and the pancreas from patients without pancreatic disease. Of
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A gene array was used to profile the expression of 22,875 long non-coding RNAs (lncRNAs) and a large number of protein coding genes in 47 specimens of pancreatic ductal adenocarcinoma (PDAC), adjacent benign pancreas and the pancreas from patients without pancreatic disease. Of the lncRNAs profiled, the expression of 126 were significantly increased and 260 were decreased in the tumors (p < 0.05, 2-fold). The expression of one lncRNA in particular, heterogeneous nuclear ribonucleoprotein U (HNRNPU) processed transcript (also known as ncRNA00201) was among the most significantly deregulated (increased four-fold) in the tumors compared to normal/adjacent benign tissues. Increased expression of HNRNPU processed transcript was associated with poor prognosis for patients with PDAC. The expression of HNRNPU processed transcript was increased in PDAC cell lines compared to noncancerous pancreatic cell lines. LNATM gapmer mediated inhibition of HNRNPU processed transcript reduced cell proliferation in Patu-T and PL45 pancreatic cancer cell lines. Reduced invasion and migration was reported upon HNRNPU processed transcript knockdown in Patu-T cells. Small interfering RNA (siRNA) knockdown of the HNRNPU protein coding gene correlated with a 55% reduction in the HNRNPU processed transcript expression and a corresponding reduction in proliferation of Patu-T and PL45 cells. However, gapmer inhibition of HNRNPU processed transcript did not affect HNRNPU mRNA levels. The lncRNA HNRNPU processed transcript expression is increased in both PDAC tissues and cell lines; knockdown of this lncRNA further reduces proliferation and invasion/migration of pancreatic carcinoma cells. Full article
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Review

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Open AccessReview miR-146 and miR-155: Two Key Modulators of Immune Response and Tumor Development
Non-Coding RNA 2017, 3(3), 22; doi:10.3390/ncrna3030022
Received: 12 May 2017 / Revised: 19 June 2017 / Accepted: 19 June 2017 / Published: 26 June 2017
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Abstract
MicroRNAs (miRNAs or miRs) are a class of evolutionarily-conserved small, regulatory non-coding RNAs, 19–3 nucleotides in length, that negatively regulate protein coding gene transcripts’ expression. miR-146 (146a and 146b) and miR-155 are among the first and most studied miRs for their multiple roles
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MicroRNAs (miRNAs or miRs) are a class of evolutionarily-conserved small, regulatory non-coding RNAs, 19–3 nucleotides in length, that negatively regulate protein coding gene transcripts’ expression. miR-146 (146a and 146b) and miR-155 are among the first and most studied miRs for their multiple roles in the control of the innate and adaptive immune processes and for their deregulation and oncogenic role in some tumors. In the present review, we have focused on the recent acquisitions about the key role played by miR-146a, miR-146b and miR-155 in the control of the immune system and in myeloid tumorigenesis. Growing experimental evidence indicates an opposite role of miR-146a with respect to miR-155 in the fine regulation of many steps of the immune response, acting at the level of the various cell types involved in innate and adaptive immune mechanisms. The demonstration that miR-155 overexpression plays a key pathogenic role in some lymphomas and acute myeloid leukemias has led to the development of an antagomir-based approach as a new promising therapeutic strategy. Full article
(This article belongs to the Special Issue ncRNAs and Cancer Immunotherapy)
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