15
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Long noncoding RNAs as regulators of cancer immunity

      review-article

      Read this article at

      Bookmark
          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

          Long noncoding RNAs (lnc RNAs) are increasingly known to be important in cancer as they directly interact with the cell cycle, proliferation pathways and microbiome balance. Moreover, lnc RNAs regulate the immune system: they do not directly encode proteins of innate or adaptive immunity, but regulate immune cell differentiation and function, such as dendritic cell activity, T cell ratio and metabolism. The result of this complex interaction is that lnc RNAs regulate cancer processes through a complex multimodal system involving immunity, metabolism and infection. The possible functions of lnc RNAs and their roles in the regulation of cancer immunity will be reported and discussed in the present review. Recent studies showed their function as regulators in the tumour microenvironment (TME), epithelial–mesenchymal transition, microbiota, metabolism and immune cell differentiation. However, there is not much knowledge regarding their roles in cancer immunity regulation. Thus, the main aim of this review is to describe lnc RNAs that have specifically been associated with immunity, the immune cycle and the TME.

          Related collections

          Most cited references54

          • Record: found
          • Abstract: found
          • Article: not found

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

          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.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Loss of FBP1 by Snail-mediated repression provides metabolic advantages in basal-like breast cancer.

            The epithelial-mesenchymal transition (EMT) enhances cancer invasiveness and confers tumor cells with cancer stem cell (CSC)-like characteristics. We show that the Snail-G9a-Dnmt1 complex, which is critical for E-cadherin promoter silencing, is also required for the promoter methylation of fructose-1,6-biphosphatase (FBP1) in basal-like breast cancer (BLBC). Loss of FBP1 induces glycolysis and results in increased glucose uptake, macromolecule biosynthesis, formation of tetrameric PKM2, and maintenance of ATP production under hypoxia. Loss of FBP1 also inhibits oxygen consumption and reactive oxygen species production by suppressing mitochondrial complex I activity; this metabolic reprogramming results in an increased CSC-like property and tumorigenicity by enhancing the interaction of β-catenin with T-cell factor. Our study indicates that the loss of FBP1 is a critical oncogenic event in EMT and BLBC. Copyright © 2013 Elsevier Inc. All rights reserved.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Coordinated circRNA Biogenesis and Function with NF90/NF110 in Viral Infection

              Circular RNAs (circRNAs) generated via back-splicing are enhanced by flanking complementary sequences. Expression levels of circRNAs vary under different conditions, suggesting participation of protein factors in their biogenesis. Using genome-wide siRNA screening that targets all human unique genes and an efficient circRNA expression reporter, we identify double-stranded RNA-binding domain containing immune factors NF90/NF110 as key regulators in circRNA biogenesis. NF90/NF110 promote circRNA production in the nucleus by associating with intronic RNA pairs juxtaposing the circRNA-forming exon(s); they also interact with mature circRNAs in the cytoplasm. Upon viral infection, circRNA expression is decreased, in part owing to the nuclear export of NF90/NF110 to the cytoplasm. Meanwhile, NF90/NF110 released from circRNP complexes bind to viral mRNAs as part of their functions in antiviral immune response. Our results therefore implicate a coordinated regulation of circRNA biogenesis and function by NF90/NF110 in viral infection.
                Bookmark

                Author and article information

                Contributors
                lonigro.c@ospedale.cuneo.it
                Journal
                Mol Oncol
                Mol Oncol
                10.1002/(ISSN)1878-0261
                MOL2
                Molecular Oncology
                John Wiley and Sons Inc. (Hoboken )
                1574-7891
                1878-0261
                13 December 2018
                January 2019
                : 13
                : 1 ( doiID: 10.1002/mol2.2019.13.issue-1 )
                : 61-73
                Affiliations
                [ 1 ] Oncology Department S. Croce & Carle Teaching Hospital Cuneo Italy
                [ 2 ] Laboratory of Clinical Trials Laboratory Department S. Croce & Carle Teaching Hospital Cuneo Italy
                Author notes
                [*] [* ] Correspondence

                C. Lo Nigro, Laboratory of Clinical Trials, Laboratory Department, S. Croce & Carle Teaching Hospital, Via Carle 5, 12100 Cuneo, Italy

                Fax: +39 0171 616331

                Tel: +39 0171 616338

                E‐mail: lonigro.c@ 123456ospedale.cuneo.it

                Article
                MOL212413
                10.1002/1878-0261.12413
                6322193
                30499165
                6f7b7c76-ecaa-4c35-89b6-35976b3d905b
                © 2018 The Authors. Published by FEBS Press and John Wiley & Sons Ltd.

                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
                : 17 August 2018
                : 09 November 2018
                : 26 November 2018
                Page count
                Figures: 2, Tables: 1, Pages: 13, Words: 8771
                Categories
                Review Article
                Review Articles
                Custom metadata
                2.0
                mol212413
                January 2019
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.5.4 mode:remove_FC converted:07.01.2019

                Oncology & Radiotherapy
                long noncoding rnas,lncrnas,cancer immunity
                Oncology & Radiotherapy
                long noncoding rnas, lncrnas, cancer immunity

                Comments

                Comment on this article