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Overexpression of survivin in primary ATL cells and sodium arsenite induces apoptosis by down-regulating survivin expression in ATL cell lines

DC FieldValueLanguage
dc.contributor.author정희철-
dc.date.accessioned2015-06-10T12:44:47Z-
dc.date.available2015-06-10T12:44:47Z-
dc.date.issued2006-
dc.identifier.issn0006-4971-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/110370-
dc.description.abstractPatients with acute- or lymphoma-type adult T-cell leukemia (ATL) have a poor outcome because of the intrinsic drug resistance to chemotherapy. Protection from apoptosis is a common feature involved in multidrug-resistance of ATL. IAP (inhibitor of apoptosis) family proteins inhibit apoptosis induced by a variety of stimuli. In this study, we investigated the expression of IAP family members (survivin, cIAP1, cIAP2, and XIAP) in the primary leukemic cells from patients with ATL. We found that survivin was overexpressed in ATL, especially in acute-type ATL. Sodium arsenite was shown to down-regulate the expression of survivin at both the protein and RNA levels in a time- and dose-dependent manner, thus inhibiting cell growth, inducing apoptosis, and enhancing the caspase-3 activity in ATL cells. Nuclear factor-κB (NF-κB) enhances the transcriptional activity of survivin. Sodium arsenite suppressed the constitutive NF-κB activation by preventing the IκB-α degradation and the nuclear translocation of NF-κB. These findings suggest that survivin is an important antiapoptotic molecule that confers drug resistance on ATL cells. Sodium arsenite was shown to down-regulate the expression of survivin through the NF-κB pathway, thus inhibiting cell growth and promoting apoptosis of ATL cells.-
dc.description.statementOfResponsibilityopen-
dc.format.extent4880~4887-
dc.relation.isPartOfBLOOD-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHActive Transport, Cell Nucleus/drug effects-
dc.subject.MESHAdult-
dc.subject.MESHAged-
dc.subject.MESHAged, 80 and over-
dc.subject.MESHAntineoplastic Combined Chemotherapy Protocols/administration & dosage-
dc.subject.MESHApoptosis/drug effects*-
dc.subject.MESHArsenites/pharmacology*-
dc.subject.MESHCell Nucleus/metabolism-
dc.subject.MESHDose-Response Relationship, Drug-
dc.subject.MESHDown-Regulation/drug effects*-
dc.subject.MESHDrug Resistance, Multiple/drug effects-
dc.subject.MESHDrug Resistance, Neoplasm/drug effects-
dc.subject.MESHEnzyme Inhibitors/pharmacology*-
dc.subject.MESHFemale-
dc.subject.MESHGene Expression Regulation, Leukemic/drug effects*-
dc.subject.MESHHumans-
dc.subject.MESHInhibitor of Apoptosis Proteins-
dc.subject.MESHJurkat Cells-
dc.subject.MESHLeukemia-Lymphoma, Adult T-Cell/drug therapy-
dc.subject.MESHLeukemia-Lymphoma, Adult T-Cell/metabolism*-
dc.subject.MESHMale-
dc.subject.MESHMicrotubule-Associated Proteins/biosynthesis*-
dc.subject.MESHMiddle Aged-
dc.subject.MESHNeoplasm Proteins/biosynthesis*-
dc.subject.MESHRNA, Neoplasm/metabolism-
dc.subject.MESHSodium Compounds/pharmacology*-
dc.subject.MESHSurvivin-
dc.subject.MESHTime Factors-
dc.subject.MESHTranscription, Genetic/drug effects-
dc.titleOverexpression of survivin in primary ATL cells and sodium arsenite induces apoptosis by down-regulating survivin expression in ATL cell lines-
dc.typeArticle-
dc.contributor.collegeResearcher Institutes (부설 연구소)-
dc.contributor.departmentCancer Metastasis Research Center (암전이연구센터)-
dc.contributor.googleauthorXiao-Fang Che-
dc.contributor.googleauthorChun-Lei Zheng-
dc.contributor.googleauthorSatsuki Owatari-
dc.contributor.googleauthorMasato Mutoh-
dc.contributor.googleauthorTakenari Gotanda-
dc.contributor.googleauthorHei-Cheul Jeung-
dc.contributor.googleauthorTatsuhiko Furukawa-
dc.contributor.googleauthorRyuji Ikeda-
dc.contributor.googleauthorMasatatsu Yamamoto-
dc.contributor.googleauthorMisako Haraguchi-
dc.contributor.googleauthorNaomichi Arima-
dc.contributor.googleauthorShin-ichi Akiyama-
dc.identifier.doi10.1182/blood-2005-08-3423-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA03794-
dc.relation.journalcodeJ00341-
dc.identifier.eissn1528-0020-
dc.identifier.pmid16497974-
dc.contributor.alternativeNameJeung, Hei Cheul-
dc.contributor.affiliatedAuthorJeung, Hei Cheul-
dc.rights.accessRightsfree-
dc.citation.volume107-
dc.citation.number12-
dc.citation.startPage4880-
dc.citation.endPage4887-
dc.identifier.bibliographicCitationBLOOD, Vol.107(12) : 4880-4887, 2006-
Appears in Collections:
5. Research Institutes (연구소) > Cancer Metastasis Research Center (암전이연구센터) > 1. Journal Papers

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