{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360004233459929856.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1038/s41388-018-0133-3"}},{"identifier":{"@type":"URI","@value":"http://www.nature.com/articles/s41388-018-0133-3"}},{"identifier":{"@type":"URI","@value":"http://www.nature.com/articles/s41388-018-0133-3.pdf"}},{"identifier":{"@type":"PMID","@value":"29507419"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"EZH2 regulates neuroblastoma cell differentiation via NTRK1 promoter epigenetic modifications"}],"description":[{"notation":[{"@value":"The polycomb repressor complex 2 molecule EZH2 is now known to play a role in essential cellular processes, namely, cell fate decisions, cell cycle regulation, senescence, cell differentiation, and cancer development/progression. EZH2 inhibitors have recently been developed; however, their effectiveness and underlying molecular mechanisms in many malignancies have not yet been elucidated in detail. Although the functional role of EZH2 in tumorigenesis in neuroblastoma (NB) has been investigated, mutations of EZH2 have not been reported. A Kaplan-Meier analysis on the event free survival and overall survival of NB patients indicated that the high expression of EZH2 correlated with an unfavorable prognosis. In order to elucidate the functional roles of EZH2 in NB tumorigenesis and its aggressiveness, we knocked down EZH2 in NB cell lines using lentivirus systems. The knockdown of EZH2 significantly induced NB cell differentiation, e.g., neurite extension, and the neuronal differentiation markers, NF68 and GAP43. EZH2 inhibitors also induced NB cell differentiation. We performed a comprehensive transcriptome analysis using Human Gene Expression Microarrays and found that NTRK1 (TrkA) is one of the EZH2-related suppression targets. The depletion of NTRK1 canceled EZH2 knockdown-induced NB cell differentiation. Our integrative methylome, transcriptome, and chromatin immunoprecipitation assays using NB cell lines and clinical samples clarified that the NTRK1 P1 and P2 promoter regions were regulated differently by DNA methylation and EZH2-related histone modifications. The NTRK1 transcript variants 1/2, which were regulated by EZH2-related H3K27me3 modifications at the P1 promoter region, were strongly expressed in favorable, but not unfavorable NB. The depletion and inhibition of EZH2 successfully induced NTRK1 transcripts and functional proteins. Collectively, these results indicate that EZH2 plays important roles in preventing the differentiation of NB cells and also that EZH2-related NTRK1 transcriptional regulation may be the key pathway for NB cell differentiation."}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380004233459929734","@type":"Researcher","foaf:name":[{"@value":"Zhenghao Li"}]},{"@id":"https://cir.nii.ac.jp/crid/1420564276176181888","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"60392247"},{"@type":"NRID","@value":"1000060392247"},{"@type":"NRID","@value":"9000017479138"},{"@type":"NRID","@value":"9000002857334"},{"@type":"NRID","@value":"9000364869213"},{"@type":"NRID","@value":"9000011233427"},{"@type":"NRID","@value":"9000391986024"},{"@type":"NRID","@value":"9000351298121"},{"@type":"NRID","@value":"9000364834013"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/read0068733"}],"foaf:name":[{"@value":"Hisanori Takenobu"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929872","@type":"Researcher","foaf:name":[{"@value":"Amallia Nuggetsiana Setyawati"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929998","@type":"Researcher","foaf:name":[{"@value":"Nobuhiro Akita"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929861","@type":"Researcher","foaf:name":[{"@value":"Masayuki Haruta"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929865","@type":"Researcher","foaf:name":[{"@value":"Shunpei Satoh"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929863","@type":"Researcher","foaf:name":[{"@value":"Yoshitaka Shinno"}]},{"@id":"https://cir.nii.ac.jp/crid/1410006817996373254","@type":"Researcher","personIdentifier":[{"@type":"NRID","@value":"9000412333795"},{"@type":"NRID","@value":"9000018918144"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/rickykc420"}],"foaf:name":[{"@value":"Koji Chikaraishi"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929874","@type":"Researcher","foaf:name":[{"@value":"Kyosuke Mukae"}]},{"@id":"https://cir.nii.ac.jp/crid/1420282801201083648","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"70795830"},{"@type":"NRID","@value":"1000070795830"}],"foaf:name":[{"@value":"Jesmin Akter"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929984","@type":"Researcher","foaf:name":[{"@value":"Ryuichi P. Sugino"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929999","@type":"Researcher","foaf:name":[{"@value":"Atsuko Nakazawa"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929996","@type":"Researcher","foaf:name":[{"@value":"Akira Nakagawara"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004233459929994","@type":"Researcher","foaf:name":[{"@value":"Hiroyuki Aburatani"}]},{"@id":"https://cir.nii.ac.jp/crid/1420845751148246272","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"20311384"},{"@type":"NRID","@value":"1000020311384"}],"foaf:name":[{"@value":"Miki Ohira"}]},{"@id":"https://cir.nii.ac.jp/crid/1420564276168161152","@type":"Researcher","personIdentifier":[{"@type":"KAKEN_RESEARCHERS","@value":"90262708"},{"@type":"NRID","@value":"1000090262708"},{"@type":"NRID","@value":"9000017479145"},{"@type":"NRID","@value":"9000001056411"},{"@type":"NRID","@value":"9000364908056"},{"@type":"NRID","@value":"9000364876921"},{"@type":"NRID","@value":"9000364875896"},{"@type":"NRID","@value":"9000256643733"},{"@type":"NRID","@value":"9000004649073"},{"@type":"NRID","@value":"9000364876460"},{"@type":"NRID","@value":"9000364878153"},{"@type":"NRID","@value":"9000255894782"},{"@type":"NRID","@value":"9000364850193"},{"@type":"NRID","@value":"9000347566137"},{"@type":"NRID","@value":"9000019239145"},{"@type":"NRID","@value":"9000412637545"},{"@type":"NRID","@value":"9000331444983"},{"@type":"NRID","@value":"9000015310432"},{"@type":"RESEARCHMAP","@value":"https://researchmap.jp/TakehikoKamijo"}],"foaf:name":[{"@value":"Takehiko Kamijo"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"09509232"},{"@type":"EISSN","@value":"14765594"}],"prism:publicationName":[{"@value":"Oncogene"}],"dc:publisher":[{"@value":"Springer Science and Business Media LLC"}],"prism:publicationDate":"2018-03-06","prism:volume":"37","prism:number":"20","prism:startingPage":"2714","prism:endingPage":"2727"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["http://creativecommons.org/licenses/by-nc-sa/4.0"],"url":[{"@id":"http://www.nature.com/articles/s41388-018-0133-3"},{"@id":"http://www.nature.com/articles/s41388-018-0133-3.pdf"}],"createdAt":"2018-03-02","modifiedAt":"2023-05-20","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Gene%20Expression%20Profiling","dc:title":"Gene Expression Profiling"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Differentiation","dc:title":"Cell Differentiation"},{"@id":"https://cir.nii.ac.jp/all?q=DNA%20Methylation","dc:title":"DNA Methylation"},{"@id":"https://cir.nii.ac.jp/all?q=Prognosis","dc:title":"Prognosis"},{"@id":"https://cir.nii.ac.jp/all?q=Survival%20Analysis","dc:title":"Survival Analysis"},{"@id":"https://cir.nii.ac.jp/all?q=Article","dc:title":"Article"},{"@id":"https://cir.nii.ac.jp/all?q=Epigenesis,%20Genetic","dc:title":"Epigenesis, Genetic"},{"@id":"https://cir.nii.ac.jp/all?q=Up-Regulation","dc:title":"Up-Regulation"},{"@id":"https://cir.nii.ac.jp/all?q=Gene%20Expression%20Regulation,%20Neoplastic","dc:title":"Gene Expression Regulation, Neoplastic"},{"@id":"https://cir.nii.ac.jp/all?q=Histone%20Code","dc:title":"Histone Code"},{"@id":"https://cir.nii.ac.jp/all?q=Histones","dc:title":"Histones"},{"@id":"https://cir.nii.ac.jp/all?q=Neuroblastoma","dc:title":"Neuroblastoma"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Line,%20Tumor","dc:title":"Cell Line, Tumor"},{"@id":"https://cir.nii.ac.jp/all?q=Gene%20Knockdown%20Techniques","dc:title":"Gene Knockdown Techniques"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Enhancer%20of%20Zeste%20Homolog%202%20Protein","dc:title":"Enhancer of Zeste Homolog 2 Protein"},{"@id":"https://cir.nii.ac.jp/all?q=Receptor,%20trkA","dc:title":"Receptor, trkA"},{"@id":"https://cir.nii.ac.jp/all?q=Promoter%20Regions,%20Genetic","dc:title":"Promoter Regions, Genetic"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Proliferation","dc:title":"Cell Proliferation"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000781915818496","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"16K10051"},{"@type":"JGN","@value":"JP16K10051"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-16K10051/"}],"notation":[{"@language":"ja","@value":"難治性神経芽腫モデルマウスを用いた単細胞解析による創薬標的スクリーニング"},{"@language":"en","@value":"Single cell screening of molecular target in using malignant neuroblastoma animal 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(CRISPR/Cas9)"}]},{"@id":"https://cir.nii.ac.jp/crid/1040282256931299072","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"17H01592"},{"@type":"JGN","@value":"JP17H01592"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17H01592/"}],"notation":[{"@language":"ja","@value":"小児悪性固形腫瘍の新規病理分子学的リスク分類の開発とゲノム診療に向けた基盤構築"},{"@language":"en","@value":"Development for a new histobiological risk stratification and establishing of genomic medicine for pediatric malignant solid tumors"}]},{"@id":"https://cir.nii.ac.jp/crid/1040282256945627392","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"17K10131"},{"@type":"JGN","@value":"JP17K10131"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K10131/"}],"notation":[{"@language":"ja","@value":"ゲノム・エピゲノム解析による難治性神経芽腫の病態理解とリスク分類法・治療法の開発"},{"@language":"en","@value":"Genomic and epigenomic profiling of high stage 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