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      Regulation of laryngeal squamous cell cancer progression by the lncRNA RP11‐159K7.2/miR‐206/DNMT3A axis

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          Abstract

          Long non‐coding RNAs (lncRNAs), which are longer than 200 nt, have been proved to play a role in promoting or inhibiting cancer progression. The following study investigated the role and underlying mechanisms of lncRNA RP11‐159K7.2 in laryngeal squamous cell carcinoma (LSCC) progression. Briefly, in situ hybridization (ISH) and real‐time quantitative PCR (RT‐qPCR) showed higher expression of RP11‐159K7.2 in LSCC tissues and cell lines. Patients with low expression level of RP11‐159K7.2 lived longer compared to those with high expression of RP11‐159K7.2 ( χ 2 = 39.111, *** P < 0.001). Multivariate Cox regression analysis suggested that lncRNA RP11‐159K7.2 was an independent prognostic factor for LSCC patients (HR = 2.961, *** P < 0.001). Furthermore, to investigate the potential involvement of RP11‐159K7.2 in the development of LSCC, we knocked out the expression of endogenous RP11‐159K7.2 in TU‐212 cells and AMC‐HN‐8 cells via CRISPR/Cas9 double vector lentiviral system. RP11‐159K7.2 knockout decreased LSCC cell growth and invasion both in vitro and in vivo. Mechanically, we found that RP11‐159K7.2 could positively regulate the expression of DNMT3A by sponging miR‐206. In addition, a feedback loop was also discovered between DNMT3A and miR‐206. To sum up, these findings suggest that lncRNA RP11‐159K7.2 could be used as a potential biomarker for prognosis and treatment of LSCC.

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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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            The Genetic Signatures of Noncoding RNAs

            John S. Mattick (2009)
            The majority of the genome in animals and plants is transcribed in a developmentally regulated manner to produce large numbers of non–protein-coding RNAs (ncRNAs), whose incidence increases with developmental complexity. There is growing evidence that these transcripts are functional, particularly in the regulation of epigenetic processes, leading to the suggestion that they compose a hitherto hidden layer of genomic programming in humans and other complex organisms. However, to date, very few have been identified in genetic screens. Here I show that this is explicable by an historic emphasis, both phenotypically and technically, on mutations in protein-coding sequences, and by presumptions about the nature of regulatory mutations. Most variations in regulatory sequences produce relatively subtle phenotypic changes, in contrast to mutations in protein-coding sequences that frequently cause catastrophic component failure. Until recently, most mapping projects have focused on protein-coding sequences, and the limited number of identified regulatory mutations have been interpreted as affecting conventional cis-acting promoter and enhancer elements, although these regions are often themselves transcribed. Moreover, ncRNA-directed regulatory circuits underpin most, if not all, complex genetic phenomena in eukaryotes, including RNA interference-related processes such as transcriptional and post-transcriptional gene silencing, position effect variegation, hybrid dysgenesis, chromosome dosage compensation, parental imprinting and allelic exclusion, paramutation, and possibly transvection and transinduction. The next frontier is the identification and functional characterization of the myriad sequence variations that influence quantitative traits, disease susceptibility, and other complex characteristics, which are being shown by genome-wide association studies to lie mostly in noncoding, presumably regulatory, regions. There is every possibility that many of these variations will alter the interactions between regulatory RNAs and their targets, a prospect that should be borne in mind in future functional analyses.
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              Emerging roles of lncRNA in cancer and therapeutic opportunities.

              Ming-Chun Jiang, Jiao-Jiao Ni, Wen-Yu Cui … (2019)
              Cancer is difficult to cure due to frequent metastasis, and developing effective therapeutic approaches to treat cancer is urgently important. Long non-coding RNAs (lncRNAs) have diverse roles in regulating gene expression at both the transcriptional and translational levels and have been reported to be involved in tumorigenesis and tumor metastasis. In this article, we review the emerging roles of lncRNAs in cancer, especially in cancer immunity, cancer metabolism and cancer metastasis. We also discuss the use of novel technologies, such as antisense oligonucleotides, CRISPR-Cas9 and nanomedicines, to target lncRNAs and thus control cancers.
              Article 0 comments Cited 205 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Yanan Sun:
                ORCID: https://orcid.org/0000-0003-4587-3297
                syn2767@126.com , Tian0041@126.com
                Journal
                Journal ID (nlm-ta): J Cell Mol Med
                Journal ID (iso-abbrev): J. Cell. Mol. Med
                Journal ID (doi): 10.1111/(ISSN)1582-4934
                Journal ID (publisher-id): JCMM
                Title: Journal of Cellular and Molecular Medicine
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 1582-1838
                ISSN (Electronic): 1582-4934
                Publication date (Electronic): 04 May 2020
                Publication date (Print): June 2020
                Volume: 24
                Issue: 12 ( doiID: 10.1111/jcmm.v24.12 )
                Pages: 6781-6795
                Affiliations
                [ 1 ] Department of Otorhinolaryngology, Head and Neck Surgery The Second Affiliated Hospital Harbin Medical University Harbin China
                [ 2 ] Department of Otorhinolaryngology, Head and Neck Surgery Puyang Oilfield General Hospital Puyang China
                [ 3 ] Department of Otorhinolaryngology Daqing Oilfield General Hospital Daqing China
                [ 4 ] Department of Otolaryngology Daqing First Hospital Daqing China
                [ 5 ] Department of Otorhinolaryngology, Head and Neck Surgery The First Affiliated Hospital Guizhou University of Traditional Chinese Medicine Guizhou China
                Author notes
                [*] [* ] Correspondence

                Yanan Sun and Linli Tian, Department of Otorhinolaryngology, The Second Affiliated Hospital, Harbin Medical University, 246 Xuefu Road, Harbin 150000, China.

                Email: syn2767@ 123456126.com (Y. S.); Tian0041@ 123456126.com (L. T.)

                Author information
                https://orcid.org/0000-0003-4587-3297
                Article
                Publisher ID: JCMM15331
                DOI: 10.1111/jcmm.15331
                PMC ID: 7299727
                PubMed ID: 32363688
                SO-VID: d42a4239-cb56-410b-8159-af8052d9aad7
                Copyright © © 2020 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 07 November 2019
                Date revision received : 27 February 2020
                Date accepted : 12 April 2020
                Page count
                Figures: 7, Tables: 3, Pages: 15, Words: 7621
                Funding
                Funded by: National Natural Science Foundation of China , open-funder-registry 10.13039/501100001809;
                Award ID: 81772874
                Award ID: 81272965
                Categories
                Subject: Original Article
                Subject: Original Articles
                Custom metadata
                source-schema-version-number 2.0
                cover-date June 2020
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.4 mode:remove_FC converted:17.06.2020

                ScienceOpen disciplines: Molecular medicine
                Keywords: crispr/cas9,dnmt3a,laryngeal squamous cell cancer (lscc),long non‐coding rna,microrna
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: crispr/cas9, dnmt3a, laryngeal squamous cell cancer (lscc), long non‐coding rna, microrna

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