Combined analysis of gene expression and genome binding profiles identified potential therapeutic targets of ciclopirox in Ewing sarcoma
Ciclopirox (CPX) is a synthetic antifungal drug that is mainly used to treat dermatomycoses. The aim of the present study was to determine whether CPX could influence Ewing sarcoma progression. The present study suggested that CPX treatment may inhibit Ewing sarcoma (ES) progression through Ewing sa...
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| Veröffentlicht in: | Molecular medicine reports 2018-03, Vol.17 (3), p.4291-4298 |
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| creator | Yuan, Baisheng Ji, Wei Xia, Haipeng Li, Jianmin |
| description | Ciclopirox (CPX) is a synthetic antifungal drug that is mainly used to treat dermatomycoses. The aim of the present study was to determine whether CPX could influence Ewing sarcoma progression. The present study suggested that CPX treatment may inhibit Ewing sarcoma (ES) progression through Ewing sarcoma breakpoint region 1‑Friend leukemia integration 1 (EWS‑FLI1), a common fusion transcript structure in patients with ES. To determine the underlying mechanisms of ES progression, cross analysis was conducted on three high‑throughput genome or transcript me datasets from the Gene Expression Omnibus. The results indicated that CPX may inhibit ES growth by affecting vasculature development and DNA replication. A combination of genome‑wide expression and binding profiles revealed several potential targets for CPX in ES, including collagen type I α2 chain, N‑myc proto‑oncogene and transforming growth factor β1, which contained significantly enriched binding peaks of FLI1. In addition, network analysis, including a protein‑protein interaction network and a transcription regulatory network, provided further detailed information about the roles of CPX in ES. This study may provide a novel solution for ES treatment and may also aid in improving its prognosis. |
| doi_str_mv | 10.3892/mmr.2018.8418 |
| format | Article |
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The aim of the present study was to determine whether CPX could influence Ewing sarcoma progression. The present study suggested that CPX treatment may inhibit Ewing sarcoma (ES) progression through Ewing sarcoma breakpoint region 1‑Friend leukemia integration 1 (EWS‑FLI1), a common fusion transcript structure in patients with ES. To determine the underlying mechanisms of ES progression, cross analysis was conducted on three high‑throughput genome or transcript me datasets from the Gene Expression Omnibus. The results indicated that CPX may inhibit ES growth by affecting vasculature development and DNA replication. A combination of genome‑wide expression and binding profiles revealed several potential targets for CPX in ES, including collagen type I α2 chain, N‑myc proto‑oncogene and transforming growth factor β1, which contained significantly enriched binding peaks of FLI1. In addition, network analysis, including a protein‑protein interaction network and a transcription regulatory network, provided further detailed information about the roles of CPX in ES. This study may provide a novel solution for ES treatment and may also aid in improving its prognosis.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.8418</identifier><identifier>PMID: 29328472</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Bioinformatics ; Cancer therapies ; Ciclopirox ; Collagen (type I) ; Datasets ; Development and progression ; DNA biosynthesis ; Drug therapy ; Ewing's sarcoma ; Ewings sarcoma ; Gene expression ; Genetic aspects ; Genomes ; Health aspects ; Leukemia ; Medical prognosis ; Myc protein ; Patient outcomes ; Protein interaction ; Transcription ; Transforming growth factor</subject><ispartof>Molecular medicine reports, 2018-03, Vol.17 (3), p.4291-4298</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Yuan et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-7b417f4b3280398b639312874bd360e769ceb92be492002047d63dae796c06843</citedby><cites>FETCH-LOGICAL-c482t-7b417f4b3280398b639312874bd360e769ceb92be492002047d63dae796c06843</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29328472$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yuan, Baisheng</creatorcontrib><creatorcontrib>Ji, Wei</creatorcontrib><creatorcontrib>Xia, Haipeng</creatorcontrib><creatorcontrib>Li, Jianmin</creatorcontrib><title>Combined analysis of gene expression and genome binding profiles identified potential therapeutic targets of ciclopirox in Ewing sarcoma</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Ciclopirox (CPX) is a synthetic antifungal drug that is mainly used to treat dermatomycoses. The aim of the present study was to determine whether CPX could influence Ewing sarcoma progression. The present study suggested that CPX treatment may inhibit Ewing sarcoma (ES) progression through Ewing sarcoma breakpoint region 1‑Friend leukemia integration 1 (EWS‑FLI1), a common fusion transcript structure in patients with ES. To determine the underlying mechanisms of ES progression, cross analysis was conducted on three high‑throughput genome or transcript me datasets from the Gene Expression Omnibus. The results indicated that CPX may inhibit ES growth by affecting vasculature development and DNA replication. A combination of genome‑wide expression and binding profiles revealed several potential targets for CPX in ES, including collagen type I α2 chain, N‑myc proto‑oncogene and transforming growth factor β1, which contained significantly enriched binding peaks of FLI1. In addition, network analysis, including a protein‑protein interaction network and a transcription regulatory network, provided further detailed information about the roles of CPX in ES. This study may provide a novel solution for ES treatment and may also aid in improving its prognosis.</description><subject>Bioinformatics</subject><subject>Cancer therapies</subject><subject>Ciclopirox</subject><subject>Collagen (type I)</subject><subject>Datasets</subject><subject>Development and progression</subject><subject>DNA biosynthesis</subject><subject>Drug therapy</subject><subject>Ewing's sarcoma</subject><subject>Ewings sarcoma</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Leukemia</subject><subject>Medical prognosis</subject><subject>Myc protein</subject><subject>Patient outcomes</subject><subject>Protein interaction</subject><subject>Transcription</subject><subject>Transforming growth factor</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptks1u1TAQhSMEoqWwZIsssWGTi2M7_tkgVVctIFViA2vLcSapq8QOdkLbN-Cxa9NLoQh54ZHnm-Ox51TV6wbvqFTk_TzHHcGN3EnWyCfVcSNUU1OM2dNDTJQSR9WLlK4w5i1p1fPqiChKJBPkuPq5D3PnPPTIeDPdJpdQGNAIHhDcLBFScsHnXF_Owgwow73zI1piGNwECbke_OoGlyWWsJbYTGi9hGgW2FZn0WriCOsvXevsFBYXww1yHp1dF6Fkog2zeVk9G8yU4NVhP6m-nZ993X-qL758_Lw_vagtk2StRccaMbAu94-pkh2nijZECtb1lGMQXFnoFOmAKYIxwUz0nPYGhOIWc8noSfXhXnfZuhl6mxuOZtJLdLOJtzoYpx9nvLvUY_ihW4kJwSQLvDsIxPB9g7Tq2SUL02Q8hC3pRknFcctpQd_-g16FLeZ_LpRigjJO2j_UaCbQzg8h32uLqD5t85i44IJmavcfKq8eZmeDhzKNxwX1fYGNIaUIw8MbG6yLdXS2ji7W0cU6mX_z98c80L-9Qu8AZQXAdA</recordid><startdate>20180301</startdate><enddate>20180301</enddate><creator>Yuan, Baisheng</creator><creator>Ji, Wei</creator><creator>Xia, Haipeng</creator><creator>Li, Jianmin</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180301</creationdate><title>Combined analysis of gene expression and genome binding profiles identified potential therapeutic targets of ciclopirox in Ewing sarcoma</title><author>Yuan, Baisheng ; Ji, Wei ; Xia, Haipeng ; Li, Jianmin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-7b417f4b3280398b639312874bd360e769ceb92be492002047d63dae796c06843</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Bioinformatics</topic><topic>Cancer therapies</topic><topic>Ciclopirox</topic><topic>Collagen (type I)</topic><topic>Datasets</topic><topic>Development and progression</topic><topic>DNA biosynthesis</topic><topic>Drug therapy</topic><topic>Ewing's sarcoma</topic><topic>Ewings sarcoma</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Health aspects</topic><topic>Leukemia</topic><topic>Medical prognosis</topic><topic>Myc protein</topic><topic>Patient outcomes</topic><topic>Protein interaction</topic><topic>Transcription</topic><topic>Transforming growth factor</topic><toplevel>online_resources</toplevel><creatorcontrib>Yuan, Baisheng</creatorcontrib><creatorcontrib>Ji, Wei</creatorcontrib><creatorcontrib>Xia, Haipeng</creatorcontrib><creatorcontrib>Li, Jianmin</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yuan, Baisheng</au><au>Ji, Wei</au><au>Xia, Haipeng</au><au>Li, Jianmin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Combined analysis of gene expression and genome binding profiles identified potential therapeutic targets of ciclopirox in Ewing sarcoma</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-03-01</date><risdate>2018</risdate><volume>17</volume><issue>3</issue><spage>4291</spage><epage>4298</epage><pages>4291-4298</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Ciclopirox (CPX) is a synthetic antifungal drug that is mainly used to treat dermatomycoses. The aim of the present study was to determine whether CPX could influence Ewing sarcoma progression. The present study suggested that CPX treatment may inhibit Ewing sarcoma (ES) progression through Ewing sarcoma breakpoint region 1‑Friend leukemia integration 1 (EWS‑FLI1), a common fusion transcript structure in patients with ES. To determine the underlying mechanisms of ES progression, cross analysis was conducted on three high‑throughput genome or transcript me datasets from the Gene Expression Omnibus. The results indicated that CPX may inhibit ES growth by affecting vasculature development and DNA replication. A combination of genome‑wide expression and binding profiles revealed several potential targets for CPX in ES, including collagen type I α2 chain, N‑myc proto‑oncogene and transforming growth factor β1, which contained significantly enriched binding peaks of FLI1. In addition, network analysis, including a protein‑protein interaction network and a transcription regulatory network, provided further detailed information about the roles of CPX in ES. This study may provide a novel solution for ES treatment and may also aid in improving its prognosis.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29328472</pmid><doi>10.3892/mmr.2018.8418</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Bioinformatics Cancer therapies Ciclopirox Collagen (type I) Datasets Development and progression DNA biosynthesis Drug therapy Ewing's sarcoma Ewings sarcoma Gene expression Genetic aspects Genomes Health aspects Leukemia Medical prognosis Myc protein Patient outcomes Protein interaction Transcription Transforming growth factor |
| title | Combined analysis of gene expression and genome binding profiles identified potential therapeutic targets of ciclopirox in Ewing sarcoma |
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