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      LncRNA2Target v2.0: a comprehensive database for target genes of lncRNAs in human and mouse

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          Abstract

          Long non-coding RNAs (lncRNAs) play crucial roles in regulating gene expression, and a growing number of researchers have focused on the identification of target genes of lncRNAs. However, no online repository is available to collect the information on target genes regulated by lncRNAs. To make it convenient for researchers to know what genes are regulated by a lncRNA of interest, we developed a database named lncRNA2Target to provide a comprehensive resource of lncRNA target genes in 2015. To update the database this year, we retrieved all new lncRNA–target relationships from papers published from 1 August 2014 to 30 April 2018 and RNA-seq datasets before and after knockdown or overexpression of a specific lncRNA. LncRNA2Target database v2.0 provides a web interface through which its users can search for the targets of a particular lncRNA or for the lncRNAs that target a particular gene, and is freely accessible at http://123.59.132.21/lncrna2target.

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          Targeting long non-coding RNAs in cancers: progress and prospects.

          Chi Han Li, Yangchao Chen (2013)
          Pervasive transcription occurs in the human genome to generate thousands of RNA transcripts, and accumulating evidence suggested that the RNA molecules, without protein coding ability, have important roles in diverse biological functions. Long non-coding RNA (lncRNA), with size larger than 200 nt, is a new class of the non-coding RNA that contributes to cancer development and progression. Roles for several lncRNAs in cancers have been characterized and strategies targeting them have inhibitory effects to malignant cells in vitro and in vivo. These findings point to the potential of lncRNAs as prospective novel therapeutic targets in cancers. Recent advance in biological drugs, led by nucleic acid drugs (i.e. siRNAs, antisense oligonucleotides), suggest directions for the development of cancer therapies targeting lncRNAs. Here, we discuss the characteristics of lncRNAs regarding their synthesis, stability and functional role in cells, and emphasize their unique properties that determine their molecular functions. We then discuss the association of lncRNAs with cancers, and illustrate the anticancer effects induced upon modulating the level and function of lncRNAs. We also revisit established methods for targeting RNA molecules and discuss new agents and strategies to attenuate lncRNAs in cancer. Copyright © 2013 Elsevier Ltd. All rights reserved.
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            Genetic variants at the 9p21 locus contribute to atherosclerosis through modulation of ANRIL and CDKN2A/B.

            Ada Congrains, Kei Kamide, Ryousuke Oguro … (2012)
            Genome-wide association studies (GWAS) have identified genetic variants contributing to the risk of cardiovascular disease (CVD) at the chromosome 9p21 locus. The CVD-associated region is adjacent to the two cyclin dependent kinase inhibitors (CDKN)2A and 2B and the last exons of the non-coding RNA, ANRIL. It is still not clear which of or how these transcripts are involved in the pathogenesis of atherosclerosis. We assessed the hypothesis that 9p21 locus polymorphisms influence the expression of the transcripts in the region (ANRIL, CDKN2A/B) and that these transcripts contribute to atherogenesis through the modulation of proliferation in VSMC. We genotyped 18 SNPs (r(2) 0.05) across the region of interest: CDKN2A/B and ANRIL, encompassing the CVD-associated region. RNA and DNA were extracted from the blood of 57 volunteers (69-72 years old). Carotid ultrasound was performed in 56 subjects. CDKN2A/B and ANRIL (exons 1-2 and 17-18) expression was measured employing RT-PCR. Gene expression and cell growth were evaluated in cultured VSMC after the siRNA-mediated knock-down of ANRIL. The risk alleles for atherosclerosis-related phenotypes were consistently associated with a lower expression of ANRIL when evaluating exons 1-2. Common carotid artery stenosis was associated with a significantly lower (P<0.01) expression of ANRIL (exons 1-2). ANRIL knock-down in VSMC caused significant variation in expression of CDKN2A/B (P<0.05) and reduction of cell growth (P<0.05) in vitro. Disease-associated SNPs at the 9p21 locus predominantly affect the expression of ANRIL. Overall, our results suggest that several CVD-associated SNPs in the 9p21 locus affect the expression of ANRIL, which, in turn modulate cell growth, possibly via CDKN2A/B regulation. Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.
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              Association of a novel long non-coding RNA in 8q24 with prostate cancer susceptibility.

              Suyoun Chung, Hidewaki Nakagawa, Motohide Uemura … (2011)
              Recent genome-wide association studies reported strong and reproducible associations of multiple genetic variants in a large "gene-desert" region of chromosome 8q24 with susceptibility to prostate cancer (PC). However, the causative or functional variants of these 8q24 loci and their biological mechanisms associated with PC susceptibility remain unclear and should be investigated. Here, focusing on its most centromeric region (so-called Region 2: Chr8: 128.14-128.28 Mb) among the multiple PC loci on 8q24, we performed fine mapping and re-sequencing of this critical region and identified SNPs (single nucleotide polymorphisms) between rs1456315 and rs7463708 (chr8: 128,173,119-128,173,237 bp) to be most significantly associated with PC susceptibility (P = 2.00 × 10(-24) , OR = 1.74, 95% confidence interval = 1.56-1.93). Importantly, we show that this region was transcribed as a ∼13 kb intron-less long non-coding RNA (ncRNA), termed PRNCR1 (prostate cancer non-coding RNA 1), and PRNCR1 expression was upregulated in some of the PC cells as well as precursor lesion prostatic intraepithelial neoplasia. Knockdown of PRNCR1 by siRNA attenuated the viability of PC cells and the transactivation activity of androgen receptor, which indicates that PRNCR1 could be involved in prostate carcinogenesis possibly through androgen receptor activity. These findings could provide a new insight in understanding the pathogenesis of genetic factors for PC susceptibility and prostate carcinogenesis. © 2010 Japanese Cancer Association.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Nucleic Acids Res
                Journal ID (iso-abbrev): Nucleic Acids Res
                Journal ID (publisher-id): nar
                Title: Nucleic Acids Research
                Publisher: Oxford University Press
                ISSN (Print): 0305-1048
                ISSN (Electronic): 1362-4962
                Publication date (Print): 08 January 2019
                Publication date (Electronic): 31 October 2018
                Publication date PMC-release: 31 October 2018
                Volume: 47
                Issue: Database issue , Database issue
                Pages: D140-D144
                Affiliations
                [1 ]College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China
                [2 ]Center for Bioinformatics, School of Life Science and Technology, Harbin Institute of Technology, Harbin 150001, China
                [3 ]Department of Radiology, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, China
                [4 ]Department of Radiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China
                Author notes
                To whom correspondence may be addressed. Tel: +86 13904509089; Fax: +86 45186297135; Email: jhjemail@ 123456163.com . Correspondence may also be addressed to Prof. Qinghua Jiang. Tel: +86 13836019402; Fax: +86 45186057695; Email: qhjiang@ 123456hit.edu.cn

                The authors wish it to be known that, in their opinion, the first three authors should be regarded as Joint First Authors.

                Author information
                http://orcid.org/0000-0002-6665-6710
                http://orcid.org/0000-0001-8888-8005
                Article
                Publisher ID: gky1051
                DOI: 10.1093/nar/gky1051
                PMC ID: 6323902
                PubMed ID: 30380072
                SO-VID: e80222e6-430b-4157-a901-b24e505173bf
                Copyright © © The Author(s) 2018. Published by Oxford University Press on behalf of Nucleic Acids Research.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial 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
                Date accepted : 26 October 2018
                Date revision received : 16 October 2018
                Date received : 17 July 2018
                Page count
                Pages: 5
                Funding
                Funded by: National Science and Technology Major Project of China
                Award ID: 2016YFC1202302
                Award ID: 2017YFC0907500
                Funded by: National Nature Science Foundation of China
                Award ID: 61571152
                Award ID: 61502125
                Award ID: 81471736
                Award ID: 81671760
                Funded by: Natural Science Foundation of Heilongjiang Province 10.13039/501100005046
                Award ID: F2015006
                Categories
                Subject: Database Issue

                ScienceOpen disciplines: Genetics
                Data availability:
                ScienceOpen disciplines: Genetics

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