27
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      lncRNASNP2: an updated database of functional SNPs and mutations in human and mouse lncRNAs

      research-article
      , , ,
      Nucleic Acids Research
      Oxford University Press

      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 non-coding RNAs (lncRNAs) are emerging as important regulators in different biological processes through various ways. Because the related data, especially mutations in cancers, increased sharply, we updated the lncRNASNP to version 2 ( http://bioinfo.life.hust.edu.cn/lncRNASNP2). lncRNASNP2 provides comprehensive information of SNPs and mutations in lncRNAs, as well as their impacts on lncRNA structure and function. lncRNASNP2 contains 7260238 SNPs on 141353 human lncRNA transcripts and 3921448 SNPs on 117405 mouse lncRNA transcripts. Besides the SNP information in the first version, the following new features were developed to improve the lncRNASNP2. (i) noncoding variants from COSMIC cancer data (859534) in lncRNAs and their effects on lncRNA structure and function; (ii) TCGA cancer mutations (315234) in lncRNAs and their impacts; (iii) lncRNA expression profiling of 20 cancer types in both tumor and its adjacent samples; (iv) expanded lncRNA-associated diseases; (v) optimized the results about lncRNAs structure change induced by variants; (vi) reduced false positives in miRNA and lncRNA interaction results. Furthermore, we developed online tools for users to analyze new variants in lncRNA. We aim to maintain the lncRNASNP as a useful resource for lncRNAs and their variants.

          Related collections

          Most cited references16

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

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

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

            Landscape of somatic mutations and clonal evolution in mantle cell lymphoma.

            Mantle cell lymphoma (MCL) is an aggressive tumor, but a subset of patients may follow an indolent clinical course. To understand the mechanisms underlying this biological heterogeneity, we performed whole-genome and/or whole-exome sequencing on 29 MCL cases and their respective matched normal DNA, as well as 6 MCL cell lines. Recurrently mutated genes were investigated by targeted sequencing in an independent cohort of 172 MCL patients. We identified 25 significantly mutated genes, including known drivers such as ataxia-telangectasia mutated (ATM), cyclin D1 (CCND1), and the tumor suppressor TP53; mutated genes encoding the anti-apoptotic protein BIRC3 and Toll-like receptor 2 (TLR2); and the chromatin modifiers WHSC1, MLL2, and MEF2B. We also found NOTCH2 mutations as an alternative phenomenon to NOTCH1 mutations in aggressive tumors with a dismal prognosis. Analysis of two simultaneous or subsequent MCL samples by whole-genome/whole-exome (n = 8) or targeted (n = 19) sequencing revealed subclonal heterogeneity at diagnosis in samples from different topographic sites and modulation of the initial mutational profile at the progression of the disease. Some mutations were predominantly clonal or subclonal, indicating an early or late event in tumor evolution, respectively. Our study identifies molecular mechanisms contributing to MCL pathogenesis and offers potential targets for therapeutic intervention.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              A pseudogene long noncoding RNA network regulates PTEN transcription and translation in human cells

              PTEN is a tumor suppressor gene that has been shown to be under the regulatory control of a PTEN pseudogene expressed noncoding RNA, PTENpg1. Here, we characterize a previously unidentified PTENpg1 encoded antisense RNA (asRNA), which regulates PTEN transcription and PTEN mRNA stability. We find two PTENpg1 asRNA isoforms, alpha and beta. The alpha isoform functions in trans, localizes to the PTEN promoter, and epigenetically modulates PTEN transcription by the recruitment of DNMT3a and EZH2. In contrast, the beta isoform interacts with PTENpg1 through an RNA:RNA pairing interaction, which affects PTEN protein output via changes of PTENpg1 stability and microRNA sponge activity. Disruption of this asRNA-regulated network induces cell cycle arrest and sensitizes cells to doxorubicin, suggesting a biological function for the respective PTENpg1 expressed asRNAs.
                Bookmark

                Author and article information

                Journal
                Nucleic Acids Res
                Nucleic Acids Res
                nar
                Nucleic Acids Research
                Oxford University Press
                0305-1048
                1362-4962
                04 January 2018
                25 October 2017
                25 October 2017
                : 46
                : Database issue , Database issue
                : D276-D280
                Affiliations
                Department of Bioinformatics and Systems Biology, Key Laboratory of Molecular Biophysics of the Ministry of Education, Hubei Bioinformatics and Molecular Imaging Key Laboratory, College of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, Hubei 430074, PR China
                Author notes
                To whom correspondence should be addressed. Tel: +86 27 8779 3177; Fax: +86 27 8779 3177; Email: guoay@ 123456mail.hust.edu.cn
                Article
                gkx1004
                10.1093/nar/gkx1004
                5753387
                29077939
                da48d2a9-a500-4300-9318-45024322eed1
                © The Author(s) 2017. Published by Oxford University Press on behalf of Nucleic Acids Research.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@ 123456oup.com

                History
                : 13 October 2017
                : 12 October 2017
                : 28 July 2017
                Page count
                Pages: 5
                Categories
                Database Issue

                Genetics
                Genetics

                Comments

                Comment on this article