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HSPB1 Inhibits the Endothelial-to-Mesenchymal Transition to Suppress Pulmonary Fibrosis and Lung Tumorigenesis.

DC FieldValueLanguage
dc.contributor.author조재호-
dc.date.accessioned2017-02-24T11:21:42Z-
dc.date.available2017-02-24T11:21:42Z-
dc.date.issued2016-
dc.identifier.issn0008-5472-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/146744-
dc.description.abstractThe endothelial-to-mesenchymal transition (EndMT) contributes to cancer, fibrosis, and other pathologic processes. However, the underlying mechanisms are poorly understood. Endothelial HSP1 (HSPB1) protects against cellular stress and has been implicated in cancer progression and pulmonary fibrosis. In this study, we investigated the role of HSPB1 in mediating the EndMT during the development of pulmonary fibrosis and lung cancer. HSPB1 silencing in human pulmonary endothelial cells accelerated emergence of the fibrotic phenotype after treatment with TGFβ or other cytokines linked to pulmonary fibrosis, suggesting that HSPB1 maintains endothelial cell identity. In mice, endothelial-specific overexpression of HSPB1 was sufficient to inhibit pulmonary fibrosis by blocking the EndMT. Conversely, HSPB1 depletion in a mouse model of lung tumorigenesis induced the EndMT. In clinical specimens of non-small cell lung cancer, HSPB1 expression was absent from tumor endothelial cells undergoing the EndMT. Our results showed that HSPB1 regulated the EndMT in lung fibrosis and cancer, suggesting that HSPB1-targeted therapeutic strategies may be applicable for treating an array of fibrotic diseases.-
dc.description.statementOfResponsibilityrestriction-
dc.format.extent1019~30-
dc.languageEnglish-
dc.publisherAmerican Association for Cancer Research-
dc.relation.isPartOfCANCER RESEARCH-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCells, Cultured-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHEpithelial-Mesenchymal Transition*/radiation effects-
dc.subject.MESHHSP27 Heat-Shock Proteins/analysis-
dc.subject.MESHHSP27 Heat-Shock Proteins/deficiency-
dc.subject.MESHHSP27 Heat-Shock Proteins/physiology*-
dc.subject.MESHHeat-Shock Proteins/analysis-
dc.subject.MESHHeat-Shock Proteins/physiology*-
dc.subject.MESHHumans-
dc.subject.MESHJanus Kinases/physiology-
dc.subject.MESHLung Neoplasms/etiology-
dc.subject.MESHLung Neoplasms/prevention & control*-
dc.subject.MESHMice-
dc.subject.MESHMice, Transgenic-
dc.subject.MESHNeoplasm Proteins/analysis-
dc.subject.MESHNeoplasm Proteins/physiology*-
dc.subject.MESHPlatelet Endothelial Cell Adhesion Molecule-1/analysis-
dc.subject.MESHPulmonary Fibrosis/etiology-
dc.subject.MESHPulmonary Fibrosis/prevention & control*-
dc.subject.MESHSTAT3 Transcription Factor/physiology-
dc.titleHSPB1 Inhibits the Endothelial-to-Mesenchymal Transition to Suppress Pulmonary Fibrosis and Lung Tumorigenesis.-
dc.typeArticle-
dc.publisher.locationUnited States-
dc.contributor.collegeCollege of Medicine-
dc.contributor.departmentDept. of Radiation Oncology-
dc.contributor.googleauthorSeo-Hyun Choi-
dc.contributor.googleauthorJae-Kyung Nam-
dc.contributor.googleauthorBu-Yeo Kim-
dc.contributor.googleauthorJunho Jang-
dc.contributor.googleauthorYoung-Bae Jin-
dc.contributor.googleauthorHae-June Lee-
dc.contributor.googleauthorSeungwoo Park-
dc.contributor.googleauthorYoung Hoon Ji-
dc.contributor.googleauthorJaeho Cho-
dc.contributor.googleauthorYoon-Jin Lee-
dc.identifier.doi10.1158/0008-5472.CAN-15-0952-
dc.contributor.localIdA03901-
dc.relation.journalcodeJ00452-
dc.identifier.eissn1538-7445-
dc.identifier.pmid26744531-
dc.identifier.urlhttp://cancerres.aacrjournals.org/content/76/5/1019-
dc.contributor.alternativeNameCho, Jae Ho-
dc.contributor.affiliatedAuthorCho, Jae Ho-
dc.citation.volume76-
dc.citation.number6-
dc.citation.startPage1019-
dc.citation.endPage30-
dc.identifier.bibliographicCitationCANCER RESEARCH, Vol.76(6) : 1019-30, 2016-
dc.date.modified2017-02-24-
dc.identifier.rimsid47487-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Radiation Oncology (방사선종양학교실) > 1. Journal Papers

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