miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes glioma growth
•High miR-96 level predicts poor prognosis of glioma.•miR-96 promotes the proliferation of glioma cells.•miR-96/Wnt/β-catenin regulatory circuitry maintains glioma cell proliferation. We found that miR-96 is overexpressed in glioma, and its level inversely correlates with the survival of patients. T...
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Veröffentlicht in: | FEBS letters 2014-08, Vol.588 (17), p.3038-3046 |
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creator | Yan, Zhiyong Wang, Jianpeng Wang, Chao Jiao, Yingbing Qi, Weiguo Che, Shusheng |
description | •High miR-96 level predicts poor prognosis of glioma.•miR-96 promotes the proliferation of glioma cells.•miR-96/Wnt/β-catenin regulatory circuitry maintains glioma cell proliferation.
We found that miR-96 is overexpressed in glioma, and its level inversely correlates with the survival of patients. The reduction in miR-96 abundance suppresses the proliferation and colony formation of glioma cells. The tumorigenicity of U-87 MG cells is reduced by miR-96 silencing. miR-96 contributes to the activation of Wnt/β-catenin pathway in glioma cells. HMG-box transcription factor 1 (HBP-1), a Wnt/β-catenin pathway inhibitor, is suppressed by miR-96. The reactivation of Wnt/β-catenin signaling causes an increase in the proliferation of glioma cells, and a decrease in miR-96 expression. On the other hand, HBP1 silencing promotes miR-96 expression. Collectively, miR-96 contributes to the progression of glioma by enhancing the activation of the Wnt/β-catenin pathway, and the miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes the proliferation of glioma cells. |
doi_str_mv | 10.1016/j.febslet.2014.06.017 |
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We found that miR-96 is overexpressed in glioma, and its level inversely correlates with the survival of patients. The reduction in miR-96 abundance suppresses the proliferation and colony formation of glioma cells. The tumorigenicity of U-87 MG cells is reduced by miR-96 silencing. miR-96 contributes to the activation of Wnt/β-catenin pathway in glioma cells. HMG-box transcription factor 1 (HBP-1), a Wnt/β-catenin pathway inhibitor, is suppressed by miR-96. The reactivation of Wnt/β-catenin signaling causes an increase in the proliferation of glioma cells, and a decrease in miR-96 expression. On the other hand, HBP1 silencing promotes miR-96 expression. Collectively, miR-96 contributes to the progression of glioma by enhancing the activation of the Wnt/β-catenin pathway, and the miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes the proliferation of glioma cells.</description><identifier>ISSN: 0014-5793</identifier><identifier>EISSN: 1873-3468</identifier><identifier>DOI: 10.1016/j.febslet.2014.06.017</identifier><identifier>PMID: 24931370</identifier><language>eng</language><publisher>England: Elsevier B.V</publisher><subject>Animals ; beta Catenin - metabolism ; Cell Line, Tumor ; Cell Proliferation ; DNA-Binding Proteins - metabolism ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Glioma ; Glioma - genetics ; Glioma - pathology ; HMG-box transcription factor 1 ; Humans ; Male ; Mice ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-96 ; Nuclear Proteins - metabolism ; Proliferation ; Survival Analysis ; Wnt Proteins - metabolism ; Wnt Signaling Pathway ; Wnt/β-catenin</subject><ispartof>FEBS letters, 2014-08, Vol.588 (17), p.3038-3046</ispartof><rights>2014 Federation of European Biochemical Societies</rights><rights>FEBS Letters 588 (2014) 1873-3468 © 2015 Federation of European Biochemical Societies</rights><rights>Copyright © 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1016%2Fj.febslet.2014.06.017$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.febslet.2014.06.017$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,1417,1433,3549,27923,27924,45573,45574,45994,46408,46832</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24931370$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yan, Zhiyong</creatorcontrib><creatorcontrib>Wang, Jianpeng</creatorcontrib><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Jiao, Yingbing</creatorcontrib><creatorcontrib>Qi, Weiguo</creatorcontrib><creatorcontrib>Che, Shusheng</creatorcontrib><title>miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes glioma growth</title><title>FEBS letters</title><addtitle>FEBS Lett</addtitle><description>•High miR-96 level predicts poor prognosis of glioma.•miR-96 promotes the proliferation of glioma cells.•miR-96/Wnt/β-catenin regulatory circuitry maintains glioma cell proliferation.
We found that miR-96 is overexpressed in glioma, and its level inversely correlates with the survival of patients. The reduction in miR-96 abundance suppresses the proliferation and colony formation of glioma cells. The tumorigenicity of U-87 MG cells is reduced by miR-96 silencing. miR-96 contributes to the activation of Wnt/β-catenin pathway in glioma cells. HMG-box transcription factor 1 (HBP-1), a Wnt/β-catenin pathway inhibitor, is suppressed by miR-96. The reactivation of Wnt/β-catenin signaling causes an increase in the proliferation of glioma cells, and a decrease in miR-96 expression. On the other hand, HBP1 silencing promotes miR-96 expression. Collectively, miR-96 contributes to the progression of glioma by enhancing the activation of the Wnt/β-catenin pathway, and the miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes the proliferation of glioma cells.</description><subject>Animals</subject><subject>beta Catenin - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Gene Silencing</subject><subject>Glioma</subject><subject>Glioma - genetics</subject><subject>Glioma - pathology</subject><subject>HMG-box transcription factor 1</subject><subject>Humans</subject><subject>Male</subject><subject>Mice</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR-96</subject><subject>Nuclear Proteins - metabolism</subject><subject>Proliferation</subject><subject>Survival Analysis</subject><subject>Wnt Proteins - metabolism</subject><subject>Wnt Signaling Pathway</subject><subject>Wnt/β-catenin</subject><issn>0014-5793</issn><issn>1873-3468</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkctuEzEUhi1ERUPhEUBZspmJj28zXiFaNQSpElULYml5PGeCo7kU29Mqr8WD8Ew4SmAJK9s6n38d_R8hb4CWQEGtdmWHTewxlYyCKKkqKVTPyALqihdcqPo5WdA8KWSl-Tl5GeOO5ncN-gU5Z0Jz4BVdkPXg7wqtVpvLW1h9G9Pq18_C2YSjH5cBt3Nv0xT2S-eDm33Kt4cwDVPCuNz2fhrschump_T9FTnrbB_x9em8IF_X11-uNsXN54-frj7cFCi4hEJ1DYKqHWOtUtK2yFshFauZ7ChQiyh511ipLDa60W3jKlYxbq1jSjVCd_yCvDvm5jV-zBiTGXx02Pd2xGmOBpQWuqb52_9RKUWuSQHL6NsTOjcDtuYh-MGGvflTUwY2R-DJ97j_OwdqDi7MzpxcmIMLQ5XJLsz6-pLdHxQcDICgVFQKctT7YxTmmh49BhOdx9Fh6wO6ZNrJ_zuX_wZof5bc</recordid><startdate>20140825</startdate><enddate>20140825</enddate><creator>Yan, Zhiyong</creator><creator>Wang, Jianpeng</creator><creator>Wang, Chao</creator><creator>Jiao, Yingbing</creator><creator>Qi, Weiguo</creator><creator>Che, Shusheng</creator><general>Elsevier B.V</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>20140825</creationdate><title>miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes glioma growth</title><author>Yan, Zhiyong ; Wang, Jianpeng ; Wang, Chao ; Jiao, Yingbing ; Qi, Weiguo ; Che, Shusheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e4351-6fbe168c22d665ade3d4562825f010aee53fba56aeb9b9dbc72723aac266b49f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Animals</topic><topic>beta Catenin - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Gene Silencing</topic><topic>Glioma</topic><topic>Glioma - genetics</topic><topic>Glioma - pathology</topic><topic>HMG-box transcription factor 1</topic><topic>Humans</topic><topic>Male</topic><topic>Mice</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR-96</topic><topic>Nuclear Proteins - metabolism</topic><topic>Proliferation</topic><topic>Survival Analysis</topic><topic>Wnt Proteins - metabolism</topic><topic>Wnt Signaling Pathway</topic><topic>Wnt/β-catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yan, Zhiyong</creatorcontrib><creatorcontrib>Wang, Jianpeng</creatorcontrib><creatorcontrib>Wang, Chao</creatorcontrib><creatorcontrib>Jiao, Yingbing</creatorcontrib><creatorcontrib>Qi, Weiguo</creatorcontrib><creatorcontrib>Che, Shusheng</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>FEBS letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yan, Zhiyong</au><au>Wang, Jianpeng</au><au>Wang, Chao</au><au>Jiao, Yingbing</au><au>Qi, Weiguo</au><au>Che, Shusheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes glioma growth</atitle><jtitle>FEBS letters</jtitle><addtitle>FEBS Lett</addtitle><date>2014-08-25</date><risdate>2014</risdate><volume>588</volume><issue>17</issue><spage>3038</spage><epage>3046</epage><pages>3038-3046</pages><issn>0014-5793</issn><eissn>1873-3468</eissn><abstract>•High miR-96 level predicts poor prognosis of glioma.•miR-96 promotes the proliferation of glioma cells.•miR-96/Wnt/β-catenin regulatory circuitry maintains glioma cell proliferation.
We found that miR-96 is overexpressed in glioma, and its level inversely correlates with the survival of patients. The reduction in miR-96 abundance suppresses the proliferation and colony formation of glioma cells. The tumorigenicity of U-87 MG cells is reduced by miR-96 silencing. miR-96 contributes to the activation of Wnt/β-catenin pathway in glioma cells. HMG-box transcription factor 1 (HBP-1), a Wnt/β-catenin pathway inhibitor, is suppressed by miR-96. The reactivation of Wnt/β-catenin signaling causes an increase in the proliferation of glioma cells, and a decrease in miR-96 expression. On the other hand, HBP1 silencing promotes miR-96 expression. Collectively, miR-96 contributes to the progression of glioma by enhancing the activation of the Wnt/β-catenin pathway, and the miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes the proliferation of glioma cells.</abstract><cop>England</cop><pub>Elsevier B.V</pub><pmid>24931370</pmid><doi>10.1016/j.febslet.2014.06.017</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals beta Catenin - metabolism Cell Line, Tumor Cell Proliferation DNA-Binding Proteins - metabolism Gene Expression Regulation, Neoplastic Gene Silencing Glioma Glioma - genetics Glioma - pathology HMG-box transcription factor 1 Humans Male Mice MicroRNAs - genetics MicroRNAs - metabolism miR-96 Nuclear Proteins - metabolism Proliferation Survival Analysis Wnt Proteins - metabolism Wnt Signaling Pathway Wnt/β-catenin |
title | miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes glioma growth |
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