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      Molecular hallmarks of long non-coding RNAs in aging and its significant effect on aging-associated diseases

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          Abstract

          Aging is linked to the deterioration of many physical and cognitive abilities and is the leading risk factor for Alzheimer’s disease. The growing aging population is a significant healthcare problem globally that researchers must investigate to better understand the underlying aging processes. Advances in microarrays and sequencing techniques have resulted in deeper analyses of diverse essential genomes (e.g., mouse, human, and rat) and their corresponding cell types, their organ-specific transcriptomes, and the tissue involved in aging. Traditional gene controllers such as DNA- and RNA-binding proteins significantly influence such programs, causing the need to sort out long non-coding RNAs, a new class of powerful gene regulatory elements. However, their functional significance in the aging process and senescence has yet to be investigated and identified. Several recent researchers have associated the initiation and development of senescence and aging in mammals with several well-reported and novel long non-coding RNAs. In this review article, we identified and analyzed the evolving functions of long non-coding RNAs in cellular processes, including cellular senescence, aging, and age-related pathogenesis, which are the major hallmarks of long non-coding RNAs in aging.

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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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            A long noncoding RNA mediates both activation and repression of immune response genes.

            Susan Carpenter, Daniel Aiello, Maninjay Atianand … (2013)
            An inducible program of inflammatory gene expression is central to antimicrobial defenses. This response is controlled by a collaboration involving signal-dependent activation of transcription factors, transcriptional co-regulators, and chromatin-modifying factors. We have identified a long noncoding RNA (lncRNA) that acts as a key regulator of this inflammatory response. Pattern recognition receptors such as the Toll-like receptors induce the expression of numerous lncRNAs. One of these, lincRNA-Cox2, mediates both the activation and repression of distinct classes of immune genes. Transcriptional repression of target genes is dependent on interactions of lincRNA-Cox2 with heterogeneous nuclear ribonucleoprotein A/B and A2/B1. Collectively, these studies unveil a central role of lincRNA-Cox2 as a broad-acting regulatory component of the circuit that controls the inflammatory response.
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              Long non-coding RNA ANRIL is required for the PRC2 recruitment to and silencing of p15(INK4B) tumor suppressor gene.

              Y Kotake, T. Nakagawa, K Kitagawa … (2011)
              A 42 kb region on human chromosome 9p21 encodes for three distinct tumor suppressors, p16(INK4A), p14(ARF) and p15(INK4B), and is altered in an estimated 30-40% of human tumors. The expression of the INK4A-ARF-INK4B gene cluster is silenced by polycomb during normal cell growth and is activated by oncogenic insults and during aging. How the polycomb is recruited to repress this gene cluster is unclear. Here, we show that expression of oncogenic Ras, which stimulates the expression of p15(INK4B) and p16(INK4A), but not p14(ARF), inhibits the expression of ANRIL (antisense non-coding RNA in the INK4 locus), a 3.8 kb-long non-coding RNA expressed in the opposite direction from INK4A-ARF-INK4B. We show that the p15(INK4B) locus is bound by SUZ12, a component of polycomb repression complex 2 (PRC2), and is H3K27-trimethylated. Notably, depletion of ANRIL disrupts the SUZ12 binding to the p15(INK4B) locus, increases the expression of p15(INK4B), but not p16(INK4A) or p14(ARF), and inhibits cellular proliferation. Finally, RNA immunoprecipitation demonstrates that ANRIL binds to SUZ12 in vivo. Collectively, these results suggest a model in which ANRIL binds to and recruits PRC2 to repress the expression of p15(INK4B) locus.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Neural Regen Res
                Journal ID (iso-abbrev): Neural Regen Res
                Journal ID (publisher-id): NRR
                Journal ID (publisher-id): Neural Regen Res
                Title: Neural Regeneration Research
                Publisher: Wolters Kluwer - Medknow (India )
                ISSN (Print): 1673-5374
                ISSN (Electronic): 1876-7958
                Publication date (Electronic, collection): May 2023
                Publication date (Electronic): 10 October 2022
                Volume: 18
                Issue: 5
                Pages: 959-968
                Affiliations
                [1 ]Department of Biological Sciences, Faculty of Basic & Applied Sciences, International Islamic University, Islamabad, Pakistan
                [2 ]Department of Biological Sciences, University of Arkansas, Fayetteville, AR, USA
                [3 ]Department of Pharmacology, Government College University, Faisalabad, Pakistan
                [4 ]Department of Bioinformatics and Biotechnology, Government College University, Faisalabad, Pakistan
                [5 ]Department of Chemistry, Chulalongkorn University, Thailand
                [6 ]Department of Neurology, Berenson-Allen Center for Noninvasive Brain Stimulation and Division of Cognitive Neurology, Beth Israel Deaconess Medical Center (KS 158), Harvard Medical School, Boston, MA, USA
                [7 ]Department of Physiology, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates
                [8 ]Department of Psychiatry, The First Hospital of Hebei Medical University, Shijiazhuang, Hebei Province, China
                [9 ]Mental Health Institute of Hebei Medical University, Shijiazhuang, Hebei Province, China
                [10 ]Neuroscience Center, King Fahad Specialist Hospital, Dammam, Saudi Arabia
                Author notes
                [* ] Correspondence to: Shahid Bashir, shahidbpk13@ 123456gmail.com .

                Author contributions: Conception, data collection, data analysis and interpretation: SAMS; data collection and writing: AA; editing & formatting: AJ; editing & critical review: MU; writing and data collection: AI, SQ; writing support: AAO; supervision and investigation: MA; revision and contribution to the final version of the manuscript: PJF, ML; critical feedback: RW; conceived of the presented idea, review the final draft, gives feedback and supervised the work: SB. All authors approved the final version of the manuscript .

                Author information
                https://orcid.org/0000-0001-6286-6895
                Article
                Publisher ID: NRR-18-959
                DOI: 10.4103/1673-5374.355751
                PMC ID: 9827784
                PubMed ID: 36254975
                SO-VID: 90284a4e-cbf3-4b1a-860e-cf79680ed8e3
                Copyright © Copyright: © Neural Regeneration Research
                License:

                This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.

                History
                Date received : 10 April 2022
                Date revision received : 23 June 2022
                Date accepted : 08 August 2022
                Categories
                Subject: Review

                Keywords: aging,alzheimer’s disease,dna sequence,epigenetics,immune,non-coding rna,oligonucleotides,telomere-associated
                Data availability:
                Keywords: aging, alzheimer’s disease, dna sequence, epigenetics, immune, non-coding rna, oligonucleotides, telomere-associated

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