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      MicroRNAs and lncRNAs in senescence: A re‐view

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          Abstract

          Cellular senescence is a stress response to a variety of extrinsic and intrinsic insults that cause genomic or epigenomic perturbations. It is now widely recognized as a potent tumor suppressor mechanism as well as a biological process impacting aging and organismal development. Like other cell fate decisions, senescence is executed and maintained by an intricate network of transcription factors (TFs), chromatin modifiers, and noncoding RNAs (ncRNAs). Altogether, these factors cooperate to implement the gene expression program that initiates and sustains the senescent phenotype. In the context of senescence, microRNAs (miRs) and long ncRNAs have been found to play regulatory roles at both the transcriptional and post‐transcriptional levels. In this review, we discuss recent developments in the field and point toward future research directions to gain a better understanding of ncRNAs in senescence. © 2015 IUBMB Life, 67(4):255–267, 2015

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          Aging, Cellular Senescence, and Cancer

          Judith Campisi (2013)
          For most species, aging promotes a host of degenerative pathologies that are characterized by debilitating losses of tissue or cellular function. However, especially among vertebrates, aging also promotes hyperplastic pathologies, the most deadly of which is cancer. In contrast to the loss of function that characterizes degenerating cells and tissues, malignant (cancerous) cells must acquire new (albeit aberrant) functions that allow them to develop into a lethal tumor. This review discusses the idea that, despite seemingly opposite characteristics, the degenerative and hyperplastic pathologies of aging are at least partly linked by a common biological phenomenon: a cellular stress response known as cellular senescence. The senescence response is widely recognized as a potent tumor suppressive mechanism. However, recent evidence strengthens the idea that it also drives both degenerative and hyperplastic pathologies, most likely by promoting chronic inflammation. Thus, the senescence response may be the result of antagonistically pleiotropic gene action.
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            Chemokine signaling via the CXCR2 receptor reinforces senescence.

            Juan C. Acosta, Ana O'Loghlen, Ana Banito … (2008)
            Cells enter senescence, a state of stable proliferative arrest, in response to a variety of cellular stresses, including telomere erosion, DNA damage, and oncogenic signaling, which acts as a barrier against malignant transformation in vivo. To identify genes controlling senescence, we conducted an unbiased screen for small hairpin RNAs that extend the life span of primary human fibroblasts. Here, we report that knocking down the chemokine receptor CXCR2 (IL8RB) alleviates both replicative and oncogene-induced senescence (OIS) and diminishes the DNA-damage response. Conversely, ectopic expression of CXCR2 results in premature senescence via a p53-dependent mechanism. Cells undergoing OIS secrete multiple CXCR2-binding chemokines in a program that is regulated by the NF-kappaB and C/EBPbeta transcription factors and coordinately induce CXCR2 expression. CXCR2 upregulation is also observed in preneoplastic lesions in vivo. These results suggest that senescent cells activate a self-amplifying secretory network in which CXCR2-binding chemokines reinforce growth arrest.
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              Molecular interplay of the noncoding RNA ANRIL and methylated histone H3 lysine 27 by polycomb CBX7 in transcriptional silencing of INK4a.

              Kyoko Yap, Side Li, Ana Muñoz-Cabello … (2010)
              Expression of the INK4b/ARF/INK4a tumor suppressor locus in normal and cancerous cell growth is controlled by methylation of histone H3 at lysine 27 (H3K27me) as directed by the Polycomb group proteins. The antisense noncoding RNA ANRIL of the INK4b/ARF/INK4a locus is also important for expression of the protein-coding genes in cis, but its mechanism has remained elusive. Here we report that chromobox 7 (CBX7) within the polycomb repressive complex 1 binds to ANRIL, and both CBX7 and ANRIL are found at elevated levels in prostate cancer tissues. In concert with H3K27me recognition, binding to RNA contributes to CBX7 function, and disruption of either interaction impacts the ability of CBX7 to repress the INK4b/ARF/INK4a locus and control senescence. Structure-guided analysis reveals the molecular interplay between noncoding RNA and H3K27me as mediated by the conserved chromodomain. Our study suggests a mechanism by which noncoding RNA participates directly in epigenetic transcriptional repression. Copyright (c) 2010 Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Journal ID (nlm-ta): IUBMB Life
                Journal ID (iso-abbrev): IUBMB Life
                Journal ID (doi): 10.1002/(ISSN)1521-6551
                Journal ID (publisher-id): IUB
                Title: Iubmb Life
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1521-6543
                ISSN (Electronic): 1521-6551
                Publication date (Electronic): 19 May 2015
                Publication date (Print): April 2015
                Volume: 67
                Issue: 4 ( doiID: 10.1002/iub.v67.4 )
                Pages: 255-267
                Affiliations
                [ 1 ]Institut Pasteur, Laboratory of Nuclear Organization and Oncogenesis Department of Cell Biology and Infection ParisFrance
                [ 2 ]INSERM U993 ParisFrance
                Author notes
                [*] [* ]Address correspondence to: Oliver Bischof, Institut Pasteur, Laboratory of Nuclear Organization and Oncogenesis, Department of Cell Biology and Infection, 75724 Paris, France. Tel: +33–140613307. Fax: +33–145688943. E‐mail: oliver.bischof@ 123456pasteur.fr
                Article
                Publisher ID: IUB1373
                DOI: 10.1002/iub.1373
                PMC ID: 5008183
                PubMed ID: 25990945
                SO-VID: ec86f2e7-b801-4d25-b886-57b106a76f32
                Copyright © © 2015 The Authors. IUBMB Life published by Wiley Periodicals, Inc. on behalf of IUBMB.
                License:

                This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 20 January 2015
                Date accepted : 16 February 2015
                Page count
                Pages: 13
                Funding
                Funded by: Fondation ARC pour la recherche sur le Cancer
                Funded by: Agence Nationale Recherche ANR
                Funded by: Pasteur‐Weizmann
                Funded by: Consejo Nacional de Ciencia y Tecnología CONACYT
                Funded by: Association LNCC La Ligue National Contre le Cancer
                Categories
                Subject: Critical Review
                Subject: Critical Reviews
                Custom metadata
                source-schema-version-number 2.0
                component-id iub1373
                cover-date April 2015
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:4.9.4 mode:remove_FC converted:01.09.2016

                Keywords: aging,senescence,transcription factors,transcriptional regulation,noncoding rna,chromatin,rna interference
                Data availability:
                Keywords: aging, senescence, transcription factors, transcriptional regulation, noncoding rna, chromatin, rna interference

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