Suppression of Disheveled–Axin Domain Containing 1 (DIXDC1) by MicroRNA-186 Inhibits the Proliferation and Invasion of Retinoblastoma Cells
Recent evidence shows that Disheveled–Axin domain containing 1 (DIXDC1) is dysregulated in various cancers. However, the role of DIXDC1 in retinoblastoma (RB) remains unclear. In this study, we aimed to investigate the biological function of DIDXDC1 in RB and the way in which its expression is regul...
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| Veröffentlicht in: | Journal of molecular neuroscience 2018-02, Vol.64 (2), p.252-261 |
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| description | Recent evidence shows that Disheveled–Axin domain containing 1 (DIXDC1) is dysregulated in various cancers. However, the role of DIXDC1 in retinoblastoma (RB) remains unclear. In this study, we aimed to investigate the biological function of DIDXDC1 in RB and the way in which its expression is regulated by microRNAs (miRNAs). We found that DIXDC1 expression was significantly upregulated in RB cell lines. The silencing of DIXDC1 by small interfering RNA (siRNA) significantly inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Interestingly, DIXDC1 was identified as a target gene of miR-186. The expression of DIXDC1 was negatively regulated by miR-186, and DIXDC1 expression was inversely correlated with miR-186 expression in RB clinical specimens. Overexpression of miR-186 inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Moreover, overexpression of DIXDC1 markedly reversed the antitumor effect of miR-186. Overall, our results reveal that DIXDC1 functions as a potential oncogene in RB, and inhibiting DIXDC1 by miR-186 suppresses the proliferation and invasion of RB cell lines. Our study suggests that DIXDC1 and miR-186 may serve as novel therapeutic targets for the treatment of RB. |
| doi_str_mv | 10.1007/s12031-017-1017-7 |
| format | Article |
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However, the role of DIXDC1 in retinoblastoma (RB) remains unclear. In this study, we aimed to investigate the biological function of DIDXDC1 in RB and the way in which its expression is regulated by microRNAs (miRNAs). We found that DIXDC1 expression was significantly upregulated in RB cell lines. The silencing of DIXDC1 by small interfering RNA (siRNA) significantly inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Interestingly, DIXDC1 was identified as a target gene of miR-186. The expression of DIXDC1 was negatively regulated by miR-186, and DIXDC1 expression was inversely correlated with miR-186 expression in RB clinical specimens. Overexpression of miR-186 inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Moreover, overexpression of DIXDC1 markedly reversed the antitumor effect of miR-186. Overall, our results reveal that DIXDC1 functions as a potential oncogene in RB, and inhibiting DIXDC1 by miR-186 suppresses the proliferation and invasion of RB cell lines. Our study suggests that DIXDC1 and miR-186 may serve as novel therapeutic targets for the treatment of RB.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-017-1017-7</identifier><identifier>PMID: 29264763</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Anticancer properties ; Antitumor activity ; Biomedical and Life Sciences ; Biomedicine ; Biotechnology ; Cancer ; Cancer therapies ; Cell Biology ; Cell Line ; Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Gene expression ; Hospitals ; Humans ; Intracellular Signaling Peptides and Proteins - genetics ; Intracellular Signaling Peptides and Proteins - metabolism ; Microfilament Proteins - genetics ; Microfilament Proteins - metabolism ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Neurochemistry ; Neurology ; Neurosciences ; Pathogenesis ; Polymerase chain reaction ; Proteins ; Proteomics ; Retina ; Retinoblastoma ; Retinoblastoma - metabolism ; Ribonucleic acid ; RNA ; Signaling ; siRNA ; Target recognition ; Tumors ; Wnt protein ; Wnt Signaling Pathway</subject><ispartof>Journal of molecular neuroscience, 2018-02, Vol.64 (2), p.252-261</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2017</rights><rights>Journal of Molecular Neuroscience is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-ecd33fd55a97c22ea41602d668f13f0cb2b23a7dff57ddcc38f14483d044ed053</citedby><cites>FETCH-LOGICAL-c372t-ecd33fd55a97c22ea41602d668f13f0cb2b23a7dff57ddcc38f14483d044ed053</cites><orcidid>0000-0003-0848-8031</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-017-1017-7$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-017-1017-7$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29264763$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Che, Xuanyi</creatorcontrib><creatorcontrib>Qian, Yuanjie</creatorcontrib><creatorcontrib>Li, Di</creatorcontrib><title>Suppression of Disheveled–Axin Domain Containing 1 (DIXDC1) by MicroRNA-186 Inhibits the Proliferation and Invasion of Retinoblastoma Cells</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>Recent evidence shows that Disheveled–Axin domain containing 1 (DIXDC1) is dysregulated in various cancers. However, the role of DIXDC1 in retinoblastoma (RB) remains unclear. In this study, we aimed to investigate the biological function of DIDXDC1 in RB and the way in which its expression is regulated by microRNAs (miRNAs). We found that DIXDC1 expression was significantly upregulated in RB cell lines. The silencing of DIXDC1 by small interfering RNA (siRNA) significantly inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Interestingly, DIXDC1 was identified as a target gene of miR-186. The expression of DIXDC1 was negatively regulated by miR-186, and DIXDC1 expression was inversely correlated with miR-186 expression in RB clinical specimens. Overexpression of miR-186 inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Moreover, overexpression of DIXDC1 markedly reversed the antitumor effect of miR-186. Overall, our results reveal that DIXDC1 functions as a potential oncogene in RB, and inhibiting DIXDC1 by miR-186 suppresses the proliferation and invasion of RB cell lines. Our study suggests that DIXDC1 and miR-186 may serve as novel therapeutic targets for the treatment of RB.</description><subject>Anticancer properties</subject><subject>Antitumor activity</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Biotechnology</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Cell Biology</subject><subject>Cell Line</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Gene expression</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins - genetics</subject><subject>Intracellular Signaling Peptides and Proteins - metabolism</subject><subject>Microfilament Proteins - genetics</subject><subject>Microfilament Proteins - metabolism</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Pathogenesis</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Proteomics</subject><subject>Retina</subject><subject>Retinoblastoma</subject><subject>Retinoblastoma - metabolism</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signaling</subject><subject>siRNA</subject><subject>Target recognition</subject><subject>Tumors</subject><subject>Wnt protein</subject><subject>Wnt Signaling Pathway</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kcFu1DAQhi1ERZeFB-CCLHEph4DHduzkuMpSWKkFVEDiZjmx03WVtRc7qdobL8CJN-RJcLQtQkgc7JFmfv__yB9Cz4C8AkLk6wSUMCgIyALmSz5ACyjLugAQ4iFakKoui0rU4hg9TumKEAocqkfomNZUcCnYAv34NO330abkgsehx2uXtvbaDtb8-v5zdeM8XoedzqUJfszV-UsM-GS9-bpu4CVub_G562K4eL8qoBJ447eudWPC49bijzEMrrdRj7O59iaPr_V90oUdnQ_toNOYE3BjhyE9QUe9HpJ9eleX6Mvpm8_Nu-Lsw9tNszorOibpWNjOMNabstS17Ci1moMg1AhR9cB60rW0pUxL0_elNKbrWO5zXjFDOLeGlGyJTg6--xi-TTaNaudSlzfQ3oYpKahlzeuyZDJLX_wjvQpT9Hm7rKoIzydDWCI4qPJfpBRtr_bR7XS8VUDUzEodWKmMSc2s1Oz8_M55anfW_HlxDycL6EGQ8shf2vhX9H9dfwPKep9D</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Che, Xuanyi</creator><creator>Qian, Yuanjie</creator><creator>Li, Di</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0848-8031</orcidid></search><sort><creationdate>20180201</creationdate><title>Suppression of Disheveled–Axin Domain Containing 1 (DIXDC1) by MicroRNA-186 Inhibits the Proliferation and Invasion of Retinoblastoma Cells</title><author>Che, Xuanyi ; Qian, Yuanjie ; Li, Di</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-ecd33fd55a97c22ea41602d668f13f0cb2b23a7dff57ddcc38f14483d044ed053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Anticancer properties</topic><topic>Antitumor activity</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Biotechnology</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Cell Biology</topic><topic>Cell Line</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Gene expression</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Intracellular Signaling Peptides and Proteins - metabolism</topic><topic>Microfilament Proteins - genetics</topic><topic>Microfilament Proteins - metabolism</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Pathogenesis</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Proteomics</topic><topic>Retina</topic><topic>Retinoblastoma</topic><topic>Retinoblastoma - metabolism</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signaling</topic><topic>siRNA</topic><topic>Target recognition</topic><topic>Tumors</topic><topic>Wnt protein</topic><topic>Wnt Signaling Pathway</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Che, Xuanyi</creatorcontrib><creatorcontrib>Qian, Yuanjie</creatorcontrib><creatorcontrib>Li, Di</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Che, Xuanyi</au><au>Qian, Yuanjie</au><au>Li, Di</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of Disheveled–Axin Domain Containing 1 (DIXDC1) by MicroRNA-186 Inhibits the Proliferation and Invasion of Retinoblastoma Cells</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>64</volume><issue>2</issue><spage>252</spage><epage>261</epage><pages>252-261</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>Recent evidence shows that Disheveled–Axin domain containing 1 (DIXDC1) is dysregulated in various cancers. However, the role of DIXDC1 in retinoblastoma (RB) remains unclear. In this study, we aimed to investigate the biological function of DIDXDC1 in RB and the way in which its expression is regulated by microRNAs (miRNAs). We found that DIXDC1 expression was significantly upregulated in RB cell lines. The silencing of DIXDC1 by small interfering RNA (siRNA) significantly inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Interestingly, DIXDC1 was identified as a target gene of miR-186. The expression of DIXDC1 was negatively regulated by miR-186, and DIXDC1 expression was inversely correlated with miR-186 expression in RB clinical specimens. Overexpression of miR-186 inhibited the proliferation, invasion, and Wnt signaling in RB cell lines. Moreover, overexpression of DIXDC1 markedly reversed the antitumor effect of miR-186. Overall, our results reveal that DIXDC1 functions as a potential oncogene in RB, and inhibiting DIXDC1 by miR-186 suppresses the proliferation and invasion of RB cell lines. Our study suggests that DIXDC1 and miR-186 may serve as novel therapeutic targets for the treatment of RB.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>29264763</pmid><doi>10.1007/s12031-017-1017-7</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-0848-8031</orcidid></addata></record> |
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| subjects | Anticancer properties Antitumor activity Biomedical and Life Sciences Biomedicine Biotechnology Cancer Cancer therapies Cell Biology Cell Line Cell Line, Tumor Cell Movement Cell Proliferation Gene expression Hospitals Humans Intracellular Signaling Peptides and Proteins - genetics Intracellular Signaling Peptides and Proteins - metabolism Microfilament Proteins - genetics Microfilament Proteins - metabolism MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Neurochemistry Neurology Neurosciences Pathogenesis Polymerase chain reaction Proteins Proteomics Retina Retinoblastoma Retinoblastoma - metabolism Ribonucleic acid RNA Signaling siRNA Target recognition Tumors Wnt protein Wnt Signaling Pathway |
| title | Suppression of Disheveled–Axin Domain Containing 1 (DIXDC1) by MicroRNA-186 Inhibits the Proliferation and Invasion of Retinoblastoma Cells |
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