ATRA-inhibited proliferation in glioma cells is associated with subcellular redistribution of β-catenin via up-regulation of Axin
Retinoic acid (RA) is a major chemopreventive agent which exerts strong anti-tumor activity partly by trans-repressing the Wnt/β-catenin signaling pathway in some tumor cell lines. However, the definite mechanism of RA trans-repression of the Wnt/β-catenin signaling pathway has not been elucidated c...
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| Veröffentlicht in: | Journal of neuro-oncology 2008-05, Vol.87 (3), p.271-277 |
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| container_title | Journal of neuro-oncology |
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| creator | Lu, Jianrong Zhang, Feng Zhao, Daqing Hong, Liu Min, Jie Zhang, Liying Li, Fanfan Yan, Yan Li, Hang Ma, Yu Li, Qing |
| description | Retinoic acid (RA) is a major chemopreventive agent which exerts strong anti-tumor activity partly by trans-repressing the Wnt/β-catenin signaling pathway in some tumor cell lines. However, the definite mechanism of RA trans-repression of the Wnt/β-catenin signaling pathway has not been elucidated clearly. In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of β-catenin. Transfecting C6 cells with rAxin further confirmed that increased expression of Axin is obligate for inhibition of proliferation and the increase of the cytoplasmic β-catenin. Our results suggested that Axin might play an important role in RA-mediated anti-proliferative effects of glioma cell lines. |
| doi_str_mv | 10.1007/s11060-008-9518-4 |
| format | Article |
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However, the definite mechanism of RA trans-repression of the Wnt/β-catenin signaling pathway has not been elucidated clearly. In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of β-catenin. Transfecting C6 cells with rAxin further confirmed that increased expression of Axin is obligate for inhibition of proliferation and the increase of the cytoplasmic β-catenin. Our results suggested that Axin might play an important role in RA-mediated anti-proliferative effects of glioma cell lines.</description><identifier>ISSN: 0167-594X</identifier><identifier>EISSN: 1573-7373</identifier><identifier>DOI: 10.1007/s11060-008-9518-4</identifier><identifier>PMID: 18217212</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Animals ; Antineoplastic Agents - pharmacology ; Axin Protein ; beta Catenin - drug effects ; beta Catenin - metabolism ; Blotting, Western ; Brain Neoplasms - drug therapy ; Brain Neoplasms - metabolism ; Cell Proliferation - drug effects ; Fluorescent Antibody Technique ; Glioma - drug therapy ; Glioma - metabolism ; Humans ; Lab. Investigation-Human/Animal Tissue ; Medicine ; Medicine & Public Health ; Neurology ; Oncology ; Protein Transport ; Rats ; Repressor Proteins - drug effects ; Repressor Proteins - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection ; Tretinoin - pharmacology ; Up-Regulation</subject><ispartof>Journal of neuro-oncology, 2008-05, Vol.87 (3), p.271-277</ispartof><rights>Springer Science+Business Media, LLC. 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342t-379ef7b5247ac6241e4a372bd2ed9449a1853f07c5c909e56083b1195c42f4213</citedby><cites>FETCH-LOGICAL-c342t-379ef7b5247ac6241e4a372bd2ed9449a1853f07c5c909e56083b1195c42f4213</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11060-008-9518-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11060-008-9518-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18217212$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lu, Jianrong</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Zhao, Daqing</creatorcontrib><creatorcontrib>Hong, Liu</creatorcontrib><creatorcontrib>Min, Jie</creatorcontrib><creatorcontrib>Zhang, Liying</creatorcontrib><creatorcontrib>Li, Fanfan</creatorcontrib><creatorcontrib>Yan, Yan</creatorcontrib><creatorcontrib>Li, Hang</creatorcontrib><creatorcontrib>Ma, Yu</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><title>ATRA-inhibited proliferation in glioma cells is associated with subcellular redistribution of β-catenin via up-regulation of Axin</title><title>Journal of neuro-oncology</title><addtitle>J Neurooncol</addtitle><addtitle>J Neurooncol</addtitle><description>Retinoic acid (RA) is a major chemopreventive agent which exerts strong anti-tumor activity partly by trans-repressing the Wnt/β-catenin signaling pathway in some tumor cell lines. However, the definite mechanism of RA trans-repression of the Wnt/β-catenin signaling pathway has not been elucidated clearly. In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of β-catenin. Transfecting C6 cells with rAxin further confirmed that increased expression of Axin is obligate for inhibition of proliferation and the increase of the cytoplasmic β-catenin. Our results suggested that Axin might play an important role in RA-mediated anti-proliferative effects of glioma cell lines.</description><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Axin Protein</subject><subject>beta Catenin - drug effects</subject><subject>beta Catenin - metabolism</subject><subject>Blotting, Western</subject><subject>Brain Neoplasms - drug therapy</subject><subject>Brain Neoplasms - metabolism</subject><subject>Cell Proliferation - drug effects</subject><subject>Fluorescent Antibody Technique</subject><subject>Glioma - drug therapy</subject><subject>Glioma - metabolism</subject><subject>Humans</subject><subject>Lab. Investigation-Human/Animal Tissue</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neurology</subject><subject>Oncology</subject><subject>Protein Transport</subject><subject>Rats</subject><subject>Repressor Proteins - drug effects</subject><subject>Repressor Proteins - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Transfection</subject><subject>Tretinoin - pharmacology</subject><subject>Up-Regulation</subject><issn>0167-594X</issn><issn>1573-7373</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kM1O3DAUha2qVZnSPgAb5FV3Lvf6J06WI8SfhFQJDRI7y3GcwSiTTO0E2i2PxIPwTDidqdh15cX5zpHvR8gRwg8E0CcJEQpgACWrFJZMfiALVFowLbT4SBaAhWaqkncH5EtKDwAgtcDP5ABLjpojX5Dn5epmyUJ_H-ow-oZu49CF1kc7hqGnoafrLgwbS53vukRDojalwQU7s09hvKdpquds6myk0TchjTHU09_20NLXF-Yy2-ehx2DptGXRrzP7L1_-Dv1X8qm1XfLf9u8huT0_W51esuufF1eny2vmhOQjE7ryra4Vl9q6gkv00grN64b7ppKyslgq0YJ2ylVQeVVAKWrESjnJW8lRHJLvu91846_Jp9FsQpr_bns_TMlwKFRRSMgg7kAXh5Sib802ho2NfwyCmcWbnXiTxZtZvJG5c7wfn-qNb94be9MZ4Dsg5ahf-2gehin2-eD_rL4BlwSQNw</recordid><startdate>20080501</startdate><enddate>20080501</enddate><creator>Lu, Jianrong</creator><creator>Zhang, Feng</creator><creator>Zhao, Daqing</creator><creator>Hong, Liu</creator><creator>Min, Jie</creator><creator>Zhang, Liying</creator><creator>Li, Fanfan</creator><creator>Yan, Yan</creator><creator>Li, Hang</creator><creator>Ma, Yu</creator><creator>Li, Qing</creator><general>Springer US</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope></search><sort><creationdate>20080501</creationdate><title>ATRA-inhibited proliferation in glioma cells is associated with subcellular redistribution of β-catenin via up-regulation of Axin</title><author>Lu, Jianrong ; Zhang, Feng ; Zhao, Daqing ; Hong, Liu ; Min, Jie ; Zhang, Liying ; Li, Fanfan ; Yan, Yan ; Li, Hang ; Ma, Yu ; Li, Qing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342t-379ef7b5247ac6241e4a372bd2ed9449a1853f07c5c909e56083b1195c42f4213</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Axin Protein</topic><topic>beta Catenin - drug effects</topic><topic>beta Catenin - metabolism</topic><topic>Blotting, Western</topic><topic>Brain Neoplasms - drug therapy</topic><topic>Brain Neoplasms - metabolism</topic><topic>Cell Proliferation - drug effects</topic><topic>Fluorescent Antibody Technique</topic><topic>Glioma - drug therapy</topic><topic>Glioma - metabolism</topic><topic>Humans</topic><topic>Lab. Investigation-Human/Animal Tissue</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Neurology</topic><topic>Oncology</topic><topic>Protein Transport</topic><topic>Rats</topic><topic>Repressor Proteins - drug effects</topic><topic>Repressor Proteins - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Transfection</topic><topic>Tretinoin - pharmacology</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lu, Jianrong</creatorcontrib><creatorcontrib>Zhang, Feng</creatorcontrib><creatorcontrib>Zhao, Daqing</creatorcontrib><creatorcontrib>Hong, Liu</creatorcontrib><creatorcontrib>Min, Jie</creatorcontrib><creatorcontrib>Zhang, Liying</creatorcontrib><creatorcontrib>Li, Fanfan</creatorcontrib><creatorcontrib>Yan, Yan</creatorcontrib><creatorcontrib>Li, Hang</creatorcontrib><creatorcontrib>Ma, Yu</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><jtitle>Journal of neuro-oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lu, Jianrong</au><au>Zhang, Feng</au><au>Zhao, Daqing</au><au>Hong, Liu</au><au>Min, Jie</au><au>Zhang, Liying</au><au>Li, Fanfan</au><au>Yan, Yan</au><au>Li, Hang</au><au>Ma, Yu</au><au>Li, Qing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ATRA-inhibited proliferation in glioma cells is associated with subcellular redistribution of β-catenin via up-regulation of Axin</atitle><jtitle>Journal of neuro-oncology</jtitle><stitle>J Neurooncol</stitle><addtitle>J Neurooncol</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>87</volume><issue>3</issue><spage>271</spage><epage>277</epage><pages>271-277</pages><issn>0167-594X</issn><eissn>1573-7373</eissn><abstract>Retinoic acid (RA) is a major chemopreventive agent which exerts strong anti-tumor activity partly by trans-repressing the Wnt/β-catenin signaling pathway in some tumor cell lines. However, the definite mechanism of RA trans-repression of the Wnt/β-catenin signaling pathway has not been elucidated clearly. In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of β-catenin. Transfecting C6 cells with rAxin further confirmed that increased expression of Axin is obligate for inhibition of proliferation and the increase of the cytoplasmic β-catenin. Our results suggested that Axin might play an important role in RA-mediated anti-proliferative effects of glioma cell lines.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>18217212</pmid><doi>10.1007/s11060-008-9518-4</doi><tpages>7</tpages></addata></record> |
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| source | MEDLINE; SpringerNature Journals |
| subjects | Animals Antineoplastic Agents - pharmacology Axin Protein beta Catenin - drug effects beta Catenin - metabolism Blotting, Western Brain Neoplasms - drug therapy Brain Neoplasms - metabolism Cell Proliferation - drug effects Fluorescent Antibody Technique Glioma - drug therapy Glioma - metabolism Humans Lab. Investigation-Human/Animal Tissue Medicine Medicine & Public Health Neurology Oncology Protein Transport Rats Repressor Proteins - drug effects Repressor Proteins - metabolism Reverse Transcriptase Polymerase Chain Reaction Transfection Tretinoin - pharmacology Up-Regulation |
| title | ATRA-inhibited proliferation in glioma cells is associated with subcellular redistribution of β-catenin via up-regulation of Axin |
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