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Apicidin potentiates the imatinib-induced apoptosis of Bcr–Abl-positive human leukaemia cells by enhancing the activation of mitochondria-dependent caspase cascades

DC FieldValueLanguage
dc.contributor.author한지숙-
dc.contributor.author고윤웅-
dc.contributor.author김진석-
dc.contributor.author맹호영-
dc.contributor.author민유홍-
dc.contributor.author이승태-
dc.contributor.author정준원-
dc.contributor.author정회경-
dc.date.accessioned2015-07-14T16:39:42Z-
dc.date.available2015-07-14T16:39:42Z-
dc.date.issued2004-
dc.identifier.issn0007-1048-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/111336-
dc.description.abstractApicidin, a histone deacetylase inhibitor, is a novel cyclic tetrapeptide with potent antiproliferative activity against various cancer cells. We examined whether apicidin potentiates the imatinib-induced apoptosis of Bcr–Abl-positive human leukaemia cells. In K562 cells, the co-administration of minimally toxic concentrations of imatinib and apicidin (imatinib/apicidin) for 48 h produced a marked increase in mitochondrial damage, processing of caspase cascades and apoptosis. Similar results were observed in leukaemic blasts obtained from patients with chronic myeloid leukaemia in blast crisis. Imatinib/apicidin co-treatment for 48 h resulted in a near complete loss of the full-length XIAP (X-linked inhibitor of apoptosis) protein, with a corresponding increase in the 29-kDa XIAP cleavage product. Both the degradation of XIAP and increased release of second mitochondria-derived activator of caspase/direct IAP-binding protein with low pI (Smac/DIABLO) into the cytosol were abrogated by pretreatment with the caspase-3 inhibitor DEVD-CHO. Imatinib/apicidin co-treatment for 48 h produced a prominent decrease in Bcr–Abl protein levels in a caspase-dependent manner. In summary, these data indicate that apicidin potentiates the imatinib-induced apoptosis of Bcr–Abl-positive leukaemia cells through the enhanced activation of the mitochondria-dependent caspase cascades, accompanied by caspase-dependent downregulation of Bcr–Abl and XIAP. These findings generate a rationale for further investigation of apicidin and imatinib as a potential therapeutic strategy in Bcr–Abl-positive leukaemias.-
dc.description.statementOfResponsibilityopen-
dc.format.extent166~178-
dc.relation.isPartOfBritish Journal of Haematology-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.titleApicidin potentiates the imatinib-induced apoptosis of Bcr–Abl-positive human leukaemia cells by enhancing the activation of mitochondria-dependent caspase cascades-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentYonsei Biomedical Research Center (연세의생명연구원)-
dc.contributor.googleauthorSeung Tae Lee-
dc.contributor.googleauthorJin Seok Kim-
dc.contributor.googleauthorYoo Hong Min-
dc.contributor.googleauthorYun Woong Ko-
dc.contributor.googleauthorJee Sook Hahn-
dc.contributor.googleauthorHoyoung Maeng-
dc.contributor.googleauthorJune-Won Cheong-
dc.contributor.googleauthorHoi Kyung Jeung-
dc.identifier.doi10.1046/j.1365-2141.2003.04759.x-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.relation.journalcodeJ00409-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1046/j.1365-2141.2003.04759.x/abstract-
dc.contributor.alternativeNameHahn, Jee Sook-
dc.contributor.alternativeNameKo, Yun Woong-
dc.contributor.alternativeNameKim, Jin Seok-
dc.contributor.alternativeNameMaeng, Ho Young-
dc.contributor.alternativeNameMin, Yoo Hong-
dc.contributor.alternativeNameLee, Seung Tae-
dc.contributor.alternativeNameCheong, June Won-
dc.contributor.alternativeNameJeung, Hoi Kyung-
dc.rights.accessRightsnot free-
dc.citation.volume124-
dc.citation.number2-
dc.citation.startPage166-
dc.citation.endPage178-
dc.identifier.bibliographicCitationBritish Journal of Haematology, Vol.124(2) : 166-178, 2004-
Appears in Collections:
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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