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      The miR-17/92 cluster: a comprehensive update on its genomics, genetics, functions and increasingly important and numerous roles in health and disease

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          The miR-17/92 cluster is among the best-studied microRNA clusters. Interest in the cluster and its members has been increasing steadily and the number of publications has grown exponentially since its discovery with more than 1000 articles published in 2012 alone. Originally found to be involved in tumorigenesis, research work in recent years has uncovered unexpected roles for its members in a wide variety of settings that include normal development, immune diseases, cardiovascular diseases, neurodegenerative diseases and aging. In light of its ever-increasing importance and ever-widening regulatory roles, we review here the latest body of knowledge on the cluster's involvement in health and disease as well as provide a novel perspective on the full spectrum of protein-coding and non-coding transcripts that are likely regulated by its members .

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          Posttranscriptional regulation of the heterochronic gene lin-14 by lin-4 mediates temporal pattern formation in C. elegans.

          Bruce Wightman, Ilho Ha, Gary Ruvkun (1993)
          During C. elegans development, the temporal pattern of many cell lineages is specified by graded activity of the heterochronic gene Lin-14. Here we demonstrate that a temporal gradient in Lin-14 protein is generated posttranscriptionally by multiple elements in the lin-14 3'UTR that are regulated by the heterochronic gene Lin-4. The lin-14 3'UTR is both necessary and sufficient to confer lin-4-mediated posttranscriptional temporal regulation. The function of the lin-14 3'UTR is conserved between C. elegans and C. briggsae. Among the conserved sequences are seven elements that are each complementary to the lin-4 RNAs. A reporter gene bearing three of these elements shows partial temporal gradient activity. These data suggest a molecular mechanism for Lin-14p temporal gradient formation: the lin-4 RNAs base pair to sites in the lin-14 3'UTR to form multiple RNA duplexes that down-regulate lin-14 translation.
          Article 0 comments Cited 1074 times – based on 0 reviews     Review now
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            A coding-independent function of gene and pseudogene mRNAs regulates tumour biology

            Laura Poliseno, Leonardo Salmena, JiangWen Zhang … (2010)
            The canonical role of messenger RNA (mRNA) is to deliver protein-coding information to sites of protein synthesis. However, given that microRNAs bind to RNAs, we hypothesized that RNAs possess a biological role in cancer cells that relies upon their ability to compete for microRNA binding and is independent of their protein-coding function. As a paradigm for the protein-coding-independent role of RNAs, we describe the functional relationship between the mRNAs produced by the PTEN tumour suppressor gene and its pseudogene (PTENP1) and the critical consequences of this interaction. We find that PTENP1 is biologically active as determined by its ability to regulate cellular levels of PTEN, and that it can exert a growth-suppressive role. We also show that PTENP1 locus is selectively lost in human cancer. We extend our analysis to other cancer-related genes that possess pseudogenes, such as oncogenic KRAS. Further, we demonstrate that the transcripts of protein coding genes such as PTEN are also biologically active. Together, these findings attribute a novel biological role to expressed pseudogenes, as they can regulate coding gene expression, and reveal a non-coding function for mRNAs.
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              Ago HITS-CLIP decodes miRNA-mRNA interaction maps

              Sung Wook Chi, Julie B. Zang, Aldo Mele … (2009)
              Summary MicroRNAs (miRNAs) play critical roles in the regulation of gene expression. However, since miRNA activity requires base pairing with only 6-8 nucleotides of mRNA, predicting target mRNAs is a major challenge. Recently, high-throughput sequencing of RNAs isolated by crosslinking immunoprecipitation (HITS-CLIP) has identified functional protein-RNA interaction sites. Here we use HITS-CLIP to covalently crosslink native Argonaute (Ago) protein-RNA complexes in mouse brain. This produced two simultaneous datasets—Ago-miRNA and Ago-mRNA binding sites—that were combined with bioinformatic analysis to identify miRNA-target mRNA interaction sites. We validated genome-wide interaction maps for miR-124, and generated additional maps for the 20 most abundant miRNAs present in P13 mouse brain. Ago HITS-CLIP provides a general platform for exploring the specificity and range of miRNA action in vivo, and identifies precise sequences for targeting clinically relevant miRNA-mRNA interactions.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cell Death Differ
                Journal ID (iso-abbrev): Cell Death Differ
                Title: Cell Death and Differentiation
                Publisher: Nature Publishing Group
                ISSN (Print): 1350-9047
                ISSN (Electronic): 1476-5403
                Publication date (Print): December 2013
                Publication date (Electronic): 11 November 2013
                Publication date PMC-release: 1 December 2013
                Volume: 20
                Issue: 12
                Pages: 1603-1614
                Affiliations
                [1 ]Computational Medicine Center, Thomas Jefferson University , Philadelphia, PA 19107, USA
                Author notes
                [* ]Computational Medicine Center, Thomas Jefferson University , 1020 Locust Street, Philadelphia, PA 19107, USA. Tel: +1 215 503-6152, Fax: +1 215 503-0466; E-mail: isidore.rigoutsos@ 123456jefferson.edu
                Article
                Publisher Item ID: cdd2013125
                DOI: 10.1038/cdd.2013.125
                PMC ID: 3824591
                PubMed ID: 24212931
                SO-VID: 812e9932-ec18-4068-8437-b4f45515e799
                Copyright © Copyright © 2013 Macmillan Publishers Limited
                License:

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

                History
                Date received : 29 April 2013
                Date revision received : 15 July 2013
                Date accepted : 19 July 2013
                Categories
                Subject: Review

                ScienceOpen disciplines: Cell biology
                Keywords: cancer,‘expanded' model of mirna targeting,microrna,mirna,oncomir,mir-17/92 cluster
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: cancer, ‘expanded' model of mirna targeting, microrna, mirna, oncomir, mir-17/92 cluster

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