Long non-coding RNA H19 promotes glioma cell invasion by deriving miR-675
H19 RNA has been characterized as an oncogenic long non-coding RNA (lncRNA) in breast and colon cancer. However, the role and function of lncRNA H19 in glioma development remain unclear. In this study, we identified that H19/miR-675 signaling was critical for glioma progression. By analyzing glioma...
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description | H19 RNA has been characterized as an oncogenic long non-coding RNA (lncRNA) in breast and colon cancer. However, the role and function of lncRNA H19 in glioma development remain unclear. In this study, we identified that H19/miR-675 signaling was critical for glioma progression. By analyzing glioma gene expression data sets, we found increased H19 in high grade gliomas. H19 depletion via siRNA inhibited invasion in glioma cells. Further, we found H19 positively correlated with its derivate miR-675 expression and reduction of H19 inhibited miR-675 expression. Bioinformatics and luciferase reporter assays showed that miR-675 modulated Cadherin 13 expression by directly targeting the binding site within the 3' UTR. Finally, introduction of miR-675 abrogated H19 knockdown-induced cell invasion inhibition in glioma cells. To our knowledge, it is first time to demonstrate that H19 regulates glioma development by deriving miR-675 and provide important clues for understanding the key roles of lncRNA-miRNA functional network in glioma. |
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However, the role and function of lncRNA H19 in glioma development remain unclear. In this study, we identified that H19/miR-675 signaling was critical for glioma progression. By analyzing glioma gene expression data sets, we found increased H19 in high grade gliomas. H19 depletion via siRNA inhibited invasion in glioma cells. Further, we found H19 positively correlated with its derivate miR-675 expression and reduction of H19 inhibited miR-675 expression. Bioinformatics and luciferase reporter assays showed that miR-675 modulated Cadherin 13 expression by directly targeting the binding site within the 3' UTR. Finally, introduction of miR-675 abrogated H19 knockdown-induced cell invasion inhibition in glioma cells. To our knowledge, it is first time to demonstrate that H19 regulates glioma development by deriving miR-675 and provide important clues for understanding the key roles of lncRNA-miRNA functional network in glioma.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0086295</identifier><identifier>PMID: 24466011</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>3' Untranslated regions ; Analysis ; Binding sites ; Bioinformatics ; Biology ; Brain cancer ; Brain Neoplasms - genetics ; Brain Neoplasms - metabolism ; Brain Neoplasms - pathology ; Brain tumors ; Breast cancer ; Cadherin ; Cadherins ; Cadherins - genetics ; Cadherins - metabolism ; Cancer genetics ; Cell Line, Tumor ; Cell Movement ; Colon ; Colon cancer ; Development and progression ; Epigenetics ; Gene expression ; Gene Expression Regulation, Neoplastic ; Genes ; Glioma ; Glioma - genetics ; Glioma - metabolism ; Glioma - pathology ; Glioma cells ; Gliomas ; Humans ; Luciferase ; Medicine ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Neoplasm Invasiveness ; Neurosurgery ; Non-coding RNA ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - physiology ; Signal Transduction ; Signaling ; siRNA</subject><ispartof>PloS one, 2014-01, Vol.9 (1), p.e86295-e86295</ispartof><rights>COPYRIGHT 2014 Public Library of Science</rights><rights>2014 Yan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2014 Yan et al 2014 Yan et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-9c1409b986a842dd7999e3a952e07719299312b0cee6f21e302de0d326b9de323</citedby><cites>FETCH-LOGICAL-c692t-9c1409b986a842dd7999e3a952e07719299312b0cee6f21e302de0d326b9de323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3900504/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3900504/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24466011$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shi, Yan</creatorcontrib><creatorcontrib>Wang, Yingyi</creatorcontrib><creatorcontrib>Luan, Wenkang</creatorcontrib><creatorcontrib>Wang, Ping</creatorcontrib><creatorcontrib>Tao, Tao</creatorcontrib><creatorcontrib>Zhang, Junxia</creatorcontrib><creatorcontrib>Qian, Jin</creatorcontrib><creatorcontrib>Liu, Ning</creatorcontrib><creatorcontrib>You, Yongping</creatorcontrib><title>Long non-coding RNA H19 promotes glioma cell invasion by deriving miR-675</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>H19 RNA has been characterized as an oncogenic long non-coding RNA (lncRNA) in breast and colon cancer. However, the role and function of lncRNA H19 in glioma development remain unclear. In this study, we identified that H19/miR-675 signaling was critical for glioma progression. By analyzing glioma gene expression data sets, we found increased H19 in high grade gliomas. H19 depletion via siRNA inhibited invasion in glioma cells. Further, we found H19 positively correlated with its derivate miR-675 expression and reduction of H19 inhibited miR-675 expression. Bioinformatics and luciferase reporter assays showed that miR-675 modulated Cadherin 13 expression by directly targeting the binding site within the 3' UTR. Finally, introduction of miR-675 abrogated H19 knockdown-induced cell invasion inhibition in glioma cells. To our knowledge, it is first time to demonstrate that H19 regulates glioma development by deriving miR-675 and provide important clues for understanding the key roles of lncRNA-miRNA functional network in glioma.</description><subject>3' Untranslated regions</subject><subject>Analysis</subject><subject>Binding sites</subject><subject>Bioinformatics</subject><subject>Biology</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain Neoplasms - metabolism</subject><subject>Brain Neoplasms - pathology</subject><subject>Brain tumors</subject><subject>Breast cancer</subject><subject>Cadherin</subject><subject>Cadherins</subject><subject>Cadherins - genetics</subject><subject>Cadherins - metabolism</subject><subject>Cancer genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Colon</subject><subject>Colon cancer</subject><subject>Development and progression</subject><subject>Epigenetics</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genes</subject><subject>Glioma</subject><subject>Glioma - 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However, the role and function of lncRNA H19 in glioma development remain unclear. In this study, we identified that H19/miR-675 signaling was critical for glioma progression. By analyzing glioma gene expression data sets, we found increased H19 in high grade gliomas. H19 depletion via siRNA inhibited invasion in glioma cells. Further, we found H19 positively correlated with its derivate miR-675 expression and reduction of H19 inhibited miR-675 expression. Bioinformatics and luciferase reporter assays showed that miR-675 modulated Cadherin 13 expression by directly targeting the binding site within the 3' UTR. Finally, introduction of miR-675 abrogated H19 knockdown-induced cell invasion inhibition in glioma cells. To our knowledge, it is first time to demonstrate that H19 regulates glioma development by deriving miR-675 and provide important clues for understanding the key roles of lncRNA-miRNA functional network in glioma.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24466011</pmid><doi>10.1371/journal.pone.0086295</doi><tpages>e86295</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 3' Untranslated regions Analysis Binding sites Bioinformatics Biology Brain cancer Brain Neoplasms - genetics Brain Neoplasms - metabolism Brain Neoplasms - pathology Brain tumors Breast cancer Cadherin Cadherins Cadherins - genetics Cadherins - metabolism Cancer genetics Cell Line, Tumor Cell Movement Colon Colon cancer Development and progression Epigenetics Gene expression Gene Expression Regulation, Neoplastic Genes Glioma Glioma - genetics Glioma - metabolism Glioma - pathology Glioma cells Gliomas Humans Luciferase Medicine MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Neoplasm Invasiveness Neurosurgery Non-coding RNA Ribonucleic acid RNA RNA, Long Noncoding - physiology Signal Transduction Signaling siRNA |
title | Long non-coding RNA H19 promotes glioma cell invasion by deriving miR-675 |
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