{"@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/1360004236802786304.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1186/bcr3668"}},{"identifier":{"@type":"URI","@value":"https://link.springer.com/content/pdf/10.1186/bcr3668.pdf"}},{"identifier":{"@type":"URI","@value":"https://link.springer.com/article/10.1186/bcr3668/fulltext.html"}},{"identifier":{"@type":"PMID","@value":"24890385"}}],"resourceType":"学術雑誌論文(journal article)","dc:title":[{"@value":"An integrated genomic approach identifies persistent tumor suppressive effects of transforming growth factor-β in human breast cancer"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title><jats:sec>\n                        <jats:title>Introduction</jats:title>\n                        <jats:p>Transforming growth factor-βs (TGF-βs) play a dual role in breast cancer, with context-dependent tumor-suppressive or pro-oncogenic effects. TGF-β antagonists are showing promise in early-phase clinical oncology trials to neutralize the pro-oncogenic effects. However, there is currently no way to determine whether the tumor-suppressive effects of TGF-β are still active in human breast tumors at the time of surgery and treatment, a situation that could lead to adverse therapeutic responses.</jats:p>\n                     </jats:sec><jats:sec>\n                        <jats:title>Methods</jats:title>\n                        <jats:p>Using a breast cancer progression model that exemplifies the dual role of TGF-β, promoter-wide chromatin immunoprecipitation and transcriptomic approaches were applied to identify a core set of TGF-β-regulated genes that specifically reflect only the tumor-suppressor arm of the pathway. The clinical significance of this signature and the underlying biology were investigated using bioinformatic analyses in clinical breast cancer datasets, and knockdown validation approaches in tumor xenografts.</jats:p>\n                     </jats:sec><jats:sec>\n                        <jats:title>Results</jats:title>\n                        <jats:p>TGF-β-driven tumor suppression was highly dependent on Smad3, and Smad3 target genes that were specifically enriched for involvement in tumor suppression were identified. Patterns of Smad3 binding reflected the preexisting active chromatin landscape, and target genes were frequently regulated in opposite directions <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo,</jats:italic> highlighting the strong contextuality of TGF-β action. An <jats:italic>in vivo-</jats:italic>weighted TGF-β/Smad3 tumor-suppressor signature was associated with good outcome in estrogen receptor-positive breast cancer cohorts. TGF-β/Smad3 effects on cell proliferation, differentiation and ephrin signaling contributed to the observed tumor suppression.</jats:p>\n                     </jats:sec><jats:sec>\n                        <jats:title>Conclusions</jats:title>\n                        <jats:p>Tumor-suppressive effects of TGF-β persist in some breast cancer patients at the time of surgery and affect clinical outcome. Carefully tailored <jats:italic>in vitro/in vivo</jats:italic> genomic approaches can identify such patients for exclusion from treatment with TGF-β antagonists.</jats:p>\n                     </jats:sec>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380004236802786452","@type":"Researcher","foaf:name":[{"@value":"Misako Sato"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786443","@type":"Researcher","foaf:name":[{"@value":"Mitsutaka Kadota"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786309","@type":"Researcher","foaf:name":[{"@value":"Binwu Tang"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786694","@type":"Researcher","foaf:name":[{"@value":"Howard H Yang"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786697","@type":"Researcher","foaf:name":[{"@value":"Yu-an Yang"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786182","@type":"Researcher","foaf:name":[{"@value":"Mengge Shan"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786566","@type":"Researcher","foaf:name":[{"@value":"Jia Weng"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786176","@type":"Researcher","foaf:name":[{"@value":"Michael A Welsh"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786564","@type":"Researcher","foaf:name":[{"@value":"Kathleen C Flanders"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786049","@type":"Researcher","foaf:name":[{"@value":"Yoshiko Nagano"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786693","@type":"Researcher","foaf:name":[{"@value":"Aleksandra M Michalowski"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786440","@type":"Researcher","foaf:name":[{"@value":"Robert J Clifford"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786569","@type":"Researcher","foaf:name":[{"@value":"Maxwell P Lee"}]},{"@id":"https://cir.nii.ac.jp/crid/1380004236802786446","@type":"Researcher","foaf:name":[{"@value":"Lalage M Wakefield"}]}],"publication":{"publicationIdentifier":[{"@type":"EISSN","@value":"1465542X"}],"prism:publicationName":[{"@value":"Breast Cancer Research"}],"dc:publisher":[{"@value":"Springer Science and Business Media LLC"}],"prism:publicationDate":"2014-06-02","prism:volume":"16","prism:number":"3","prism:startingPage":"R57"},"reviewed":"false","dcterms:accessRights":"http://purl.org/coar/access_right/c_abf2","dc:rights":["http://creativecommons.org/licenses/by/2.0/","http://creativecommons.org/licenses/by/2.0/"],"url":[{"@id":"https://link.springer.com/content/pdf/10.1186/bcr3668.pdf"},{"@id":"https://link.springer.com/article/10.1186/bcr3668/fulltext.html"}],"createdAt":"2014-06-02","modifiedAt":"2024-10-08","foaf:topic":[{"@id":"https://cir.nii.ac.jp/all?q=Medicine(all)","dc:title":"Medicine(all)"},{"@id":"https://cir.nii.ac.jp/all?q=Receptor,%20EphA2","dc:title":"Receptor, EphA2"},{"@id":"https://cir.nii.ac.jp/all?q=Tumor%20Suppressor%20Proteins","dc:title":"Tumor Suppressor Proteins"},{"@id":"https://cir.nii.ac.jp/all?q=Breast%20Neoplasms","dc:title":"Breast Neoplasms"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Differentiation","dc:title":"Cell Differentiation"},{"@id":"https://cir.nii.ac.jp/all?q=Smad2%20Protein","dc:title":"Smad2 Protein"},{"@id":"https://cir.nii.ac.jp/all?q=Transforming%20Growth%20Factor%20beta","dc:title":"Transforming Growth Factor beta"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Line,%20Tumor","dc:title":"Cell Line, Tumor"},{"@id":"https://cir.nii.ac.jp/all?q=Humans","dc:title":"Humans"},{"@id":"https://cir.nii.ac.jp/all?q=Female","dc:title":"Female"},{"@id":"https://cir.nii.ac.jp/all?q=RNA%20Interference","dc:title":"RNA Interference"},{"@id":"https://cir.nii.ac.jp/all?q=Smad3%20Protein","dc:title":"Smad3 Protein"},{"@id":"https://cir.nii.ac.jp/all?q=RNA,%20Small%20Interfering","dc:title":"RNA, Small Interfering"},{"@id":"https://cir.nii.ac.jp/all?q=Promoter%20Regions,%20Genetic","dc:title":"Promoter Regions, Genetic"},{"@id":"https://cir.nii.ac.jp/all?q=Ephrins","dc:title":"Ephrins"},{"@id":"https://cir.nii.ac.jp/all?q=Research%20Article","dc:title":"Research Article"},{"@id":"https://cir.nii.ac.jp/all?q=Cell%20Proliferation","dc:title":"Cell Proliferation"}],"project":[{"@id":"https://cir.nii.ac.jp/crid/1040000782276742528","@type":"Project","projectIdentifier":[{"@type":"KAKEN","@value":"25871241"},{"@type":"JGN","@value":"JP25871241"},{"@type":"URI","@value":"https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-25871241/"}],"notation":[{"@language":"ja","@value":"マルチオミックス解析によるTGF-β癌促進作用機序の解明"},{"@language":"en","@value":"Differential proteome analysis identifies TGF-beta related pro-metastatic proteins in a 4T1 murine breast cancer model"}]}],"relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1050866647413161984","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@language":"en","@value":"Receptor-activated transcription 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