For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
41
views
108
references
 Top references
cited by
101
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      985
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      MALAT1: a druggable long non-coding RNA for targeted anti-cancer approaches

      review-article

      Read this article at

      ScienceOpenPublisherPMC
      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

          The deeper understanding of non-coding RNAs has recently changed the dogma of molecular biology assuming protein-coding genes as unique functional biological effectors, while non-coding genes as junk material of doubtful significance. In the last decade, an exciting boom of experimental research has brought to light the pivotal biological functions of long non-coding RNAs (lncRNAs), representing more than the half of the whole non-coding transcriptome, along with their dysregulation in many diseases, including cancer.

          In this review, we summarize the emerging insights on lncRNA expression and functional role in cancer, focusing on the evolutionary conserved and abundantly expressed metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) that currently represents the best characterized lncRNA. Altogether, literature data indicate aberrant expression and dysregulated activity of MALAT1 in human malignancies and envision MALAT1 targeting as a novel treatment strategy against cancer.

          Related collections

          Most cited references108

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

          Targeting microRNAs in cancer: rationale, strategies and challenges.

          Ramiro Garzon, Guido Marcucci, Carlo Croce (2010)
          MicroRNAs (miRNAs) are evolutionarily conserved small non-coding RNAs that regulate gene expression. Early studies have shown that miRNA expression is deregulated in cancer and experimental data indicate that cancer phenotypes can be modified by targeting miRNA expression. Based on these observations, miRNA-based anticancer therapies are being developed, either alone or in combination with current targeted therapies, with the goal to improve disease response and increase cure rates. The advantage of using miRNA approaches is based on its ability to concurrently target multiple effectors of pathways involved in cell differentiation, proliferation and survival. In this Review, we describe the role of miRNAs in tumorigenesis and critically discuss the rationale, the strategies and the challenges for the therapeutic targeting of miRNAs in cancer.
          Article 0 comments Cited 513 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Whole-genome mutational landscape and characterization of noncoding and structural mutations in liver cancer.

            Akihiro Fujimoto, Mayuko Furuta, Yasushi Totoki … (2016)
            Liver cancer, which is most often associated with virus infection, is prevalent worldwide, and its underlying etiology and genomic structure are heterogeneous. Here we provide a whole-genome landscape of somatic alterations in 300 liver cancers from Japanese individuals. Our comprehensive analysis identified point mutations, structural variations (STVs), and virus integrations, in noncoding and coding regions. We discovered mutational signatures related to liver carcinogenesis and recurrently mutated coding and noncoding regions, such as long intergenic noncoding RNA genes (NEAT1 and MALAT1), promoters, CTCF-binding sites, and regulatory regions. STV analysis found a significant association with replication timing and identified known (CDKN2A, CCND1, APC, and TERT) and new (ASH1L, NCOR1, and MACROD2) cancer-related genes that were recurrently affected by STVs, leading to altered expression. These results emphasize the value of whole-genome sequencing analysis in discovering cancer driver mutations and understanding comprehensive molecular profiles of liver cancer, especially with regard to STVs and noncoding mutations.
            Article 0 comments Cited 362 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Repression of the human dihydrofolate reductase gene by a non-coding interfering transcript.

              Igor Martianov, Aroul Ramadass, Ana Serra Barros … (2007)
              Alternative promoters within the same gene are a general phenomenon in gene expression. Mechanisms of their selective regulation vary from one gene to another and are still poorly understood. Here we show that in quiescent cells the mechanism of transcriptional repression of the major promoter of the gene encoding dihydrofolate reductase depends on a non-coding transcript initiated from the upstream minor promoter and involves both the direct interaction of the RNA and promoter-specific interference. The specificity and efficiency of repression is ensured by the formation of a stable complex between non-coding RNA and the major promoter, direct interaction of the non-coding RNA with the general transcription factor IIB and dissociation of the preinitiation complex from the major promoter. By using in vivo and in vitro assays such as inducible and reconstituted transcription, RNA bandshifts, RNA interference, chromatin immunoprecipitation and RNA immunoprecipitation, we show that the regulatory transcript produced from the minor promoter has a critical function in an epigenetic mechanism of promoter-specific transcriptional repression.
              Article 0 comments Cited 265 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Nicola Amodio:
                ORCID: http://orcid.org/0000-0001-6061-626X
                +39-0961-3694159 , amodio@unicz.it
                Pierfrancesco Tassone: tassone@unicz.it
                Journal
                Journal ID (nlm-ta): J Hematol Oncol
                Journal ID (iso-abbrev): J Hematol Oncol
                Title: Journal of Hematology & Oncology
                Publisher: BioMed Central (London )
                ISSN (Electronic): 1756-8722
                Publication date (Electronic): 8 May 2018
                Publication date PMC-release: 8 May 2018
                Publication date Collection: 2018
                Volume: 11
                Electronic Location Identifier: 63
                Affiliations
                [1 ]ISNI 0000 0001 2168 2547, GRID grid.411489.1, Department of Experimental and Clinical Medicine, , Magna Graecia University, ; Viale Europa, 88100 Catanzaro, Italy
                [2 ]ISNI 0000 0001 2154 6641, GRID grid.419038.7, IRCSS Rizzoli Orthopedic Institute, ; Bologna, Italy
                [3 ]Innovative Technology Platforms for Tissue Engineering, Theranostic and Oncology, Rizzoli Orthopedic Institute, Palermo, Italy
                Author information
                http://orcid.org/0000-0001-6061-626X
                Article
                Publisher ID: 606
                DOI: 10.1186/s13045-018-0606-4
                PMC ID: 5941496
                PubMed ID: 29739426
                SO-VID: b2024828-9960-4123-82ba-3e47d14a197b
                Copyright © © The Author(s). 2018
                License:

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                History
                Date received : 21 February 2018
                Date accepted : 26 April 2018
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: malat1,long non-coding rna,lncrna,non-coding rna,epigenetics,experimental therapeutics
                Data availability:
                ScienceOpen disciplines: Oncology & Radiotherapy
                Keywords: malat1, long non-coding rna, lncrna, non-coding rna, epigenetics, experimental therapeutics

                Comments

                Comment on this article

                scite_

                Similar content985

                See all similar

                Cited by140

                See all cited by

                Most referenced authors3,125

                See all reference authors