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Proto-oncogene FBI-1 represses transcription of p21CIP1 by inhibition of transcription activation by p53 and Sp1

DC FieldValueLanguage
dc.contributor.author윤채옥-
dc.contributor.author전부남-
dc.contributor.author최원일-
dc.contributor.author허만욱-
dc.contributor.author김세훈-
dc.contributor.author김평환-
dc.date.accessioned2015-04-24T16:23:27Z-
dc.date.available2015-04-24T16:23:27Z-
dc.date.issued2009-
dc.identifier.issn0021-9258-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/103426-
dc.description.abstractAberrant transcriptional repression through chromatin remodeling and histone deacetylation has been postulated as the driving force for tumorigenesis. FBI-1 (formerly called Pokemon) is a member of the POK family of transcriptional repressors. Recently, FBI-1 was characterized as a critical oncogenic factor that specifically represses transcription of the tumor suppressor gene ARF, potentially leading indirectly to p53 inactivation. Our investigations on transcriptional repression of the p53 pathway revealed that FBI-1 represses transcription of ARF, Hdm2 (human analogue of mouse double minute oncogene), and p21CIP1 (hereafter indicated as p21) but not of p53. FBI-1 showed a more potent repressive effect on p21 than on p53. Our data suggested that FBI-1 is a master controller of the ARF-Hdm2-p53-p21 pathway, ultimately impinging on cell cycle arrest factor p21, by inhibiting upstream regulators at the transcriptional and protein levels. FBI-1 acted as a competitive transcriptional repressor of p53 and Sp1 and was shown to bind the proximal Sp1-3 GC-box and the distal p53-responsive elements of p21. Repression involved direct binding competition of FBI-1 with Sp1 and p53. FBI-1 also interacted with corepressors, such as mSin3A, NCoR, and SMRT, thereby deacetylating Ac-H3 and Ac-H4 histones at the promoter. FBI-1 caused cellular transformation, promoted cell cycle proliferation, and significantly increased the number of cells in S phase. FBI-1 is aberrantly overexpressed in many human solid tumors, particularly in adenocarcinomas and squamous carcinomas. The role of FBI-1 as a master controller of the p53 pathway therefore makes it an attractive therapeutic target.-
dc.description.statementOfResponsibilityopen-
dc.format.extent12633~12644-
dc.relation.isPartOfJOURNAL OF BIOLOGICAL CHEMISTRY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHBlotting, Western-
dc.subject.MESHBone Neoplasms/genetics-
dc.subject.MESHBone Neoplasms/metabolism-
dc.subject.MESHBone Neoplasms/pathology-
dc.subject.MESHCell Cycle-
dc.subject.MESHCell Proliferation-
dc.subject.MESHChromatin Immunoprecipitation-
dc.subject.MESHColony-Forming Units Assay-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p21/antagonists & inhibitors-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p21/genetics*-
dc.subject.MESHCyclin-Dependent Kinase Inhibitor p21/metabolism-
dc.subject.MESHDNA-Binding Proteins/physiology*-
dc.subject.MESHElectrophoretic Mobility Shift Assay-
dc.subject.MESHFlow Cytometry-
dc.subject.MESHGene Expression Regulation, Neoplastic*-
dc.subject.MESHHeLa Cells-
dc.subject.MESHHumans-
dc.subject.MESHImmunoprecipitation-
dc.subject.MESHMutagenesis, Site-Directed-
dc.subject.MESHOsteosarcoma/genetics-
dc.subject.MESHOsteosarcoma/metabolism-
dc.subject.MESHOsteosarcoma/pathology-
dc.subject.MESHPromoter Regions, Genetic-
dc.subject.MESHRNA, Small Interfering/pharmacology-
dc.subject.MESHSp1 Transcription Factor/genetics*-
dc.subject.MESHTranscription Factors/physiology*-
dc.subject.MESHTranscription, Genetic/drug effects*-
dc.subject.MESHTranscriptional Activation/drug effects*-
dc.subject.MESHTumor Cells, Cultured-
dc.subject.MESHTumor Suppressor Protein p53/genetics*-
dc.titleProto-oncogene FBI-1 represses transcription of p21CIP1 by inhibition of transcription activation by p53 and Sp1-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Pathology (병리학)-
dc.contributor.googleauthorWon-Il Choi-
dc.contributor.googleauthorBu-Nam Jeon-
dc.contributor.googleauthorChae-Ok Yun-
dc.contributor.googleauthorPyung-Hwan Kim-
dc.contributor.googleauthorSung-Eun Kim-
dc.contributor.googleauthorKang-Yell Choi-
dc.contributor.googleauthorSe Hoon Kim-
dc.contributor.googleauthorMan-Wook Hur-
dc.identifier.doi10.1074/jbc.M809794200-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02614-
dc.contributor.localIdA03517-
dc.contributor.localIdA04126-
dc.contributor.localIdA04350-
dc.contributor.localIdA00610-
dc.contributor.localIdA01088-
dc.relation.journalcodeJ01258-
dc.identifier.eissn1083-351X-
dc.identifier.pmid19244234-
dc.contributor.alternativeNameYun, Chae Ok-
dc.contributor.alternativeNameJeon, Bu Nam-
dc.contributor.alternativeNameChoi, Won Il-
dc.contributor.alternativeNameHur, Man Wook-
dc.contributor.alternativeNameKim, Se Hoon-
dc.contributor.alternativeNameKim, Pyung Hwan-
dc.contributor.affiliatedAuthorYun, Chae Ok-
dc.contributor.affiliatedAuthorJeon, Bu Nam-
dc.contributor.affiliatedAuthorChoi, Won Il-
dc.contributor.affiliatedAuthorHur, Man Wook-
dc.contributor.affiliatedAuthorKim, Se Hoon-
dc.contributor.affiliatedAuthorKim, Pyung Hwan-
dc.citation.volume284-
dc.citation.number19-
dc.citation.startPage12633-
dc.citation.endPage12644-
dc.identifier.bibliographicCitationJOURNAL OF BIOLOGICAL CHEMISTRY, Vol.284(19) : 12633-12644, 2009-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Pathology (병리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Medical Research Center (임상의학연구센터) > 1. Journal Papers
5. Research Institutes (연구소) > Institute for Cancer Research (암연구소) > 1. Journal Papers

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