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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 Field | Value | Language |
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dc.contributor.author | 한지숙 | - |
dc.contributor.author | 고윤웅 | - |
dc.contributor.author | 김진석 | - |
dc.contributor.author | 맹호영 | - |
dc.contributor.author | 민유홍 | - |
dc.contributor.author | 이승태 | - |
dc.contributor.author | 정준원 | - |
dc.contributor.author | 정회경 | - |
dc.date.accessioned | 2015-07-14T16:39:42Z | - |
dc.date.available | 2015-07-14T16:39:42Z | - |
dc.date.issued | 2004 | - |
dc.identifier.issn | 0007-1048 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/111336 | - |
dc.description.abstract | Apicidin, 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.statementOfResponsibility | open | - |
dc.format.extent | 166~178 | - |
dc.relation.isPartOf | BRITISH JOURNAL OF HAEMATOLOGY | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Antineoplastic Combined Chemotherapy Protocols/therapeutic use* | - |
dc.subject.MESH | Apoptosis/drug effects | - |
dc.subject.MESH | Benzamides | - |
dc.subject.MESH | Blotting, Western | - |
dc.subject.MESH | Caspases/metabolism* | - |
dc.subject.MESH | Drug Synergism | - |
dc.subject.MESH | Enzyme Inhibitors/therapeutic use* | - |
dc.subject.MESH | Genes, abl | - |
dc.subject.MESH | Histone Deacetylase Inhibitors | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Imatinib Mesylate | - |
dc.subject.MESH | K562Cells | - |
dc.subject.MESH | Leukemia, Myelogenous, Chronic,BCR-ABL Positive/drug therapy* | - |
dc.subject.MESH | Leukemia, Myelogenous, Chronic,BCR-ABL Positive/enzymology | - |
dc.subject.MESH | Leukemia, Myelogenous, Chronic,BCR-ABL Positive/pathology | - |
dc.subject.MESH | Mitochondria/enzymology | - |
dc.subject.MESH | Peptides, Cyclic/administration & dosage* | - |
dc.subject.MESH | Piperazines/administration & dosage* | - |
dc.subject.MESH | Pyrimidines/administration & dosage* | - |
dc.title | Apicidin potentiates the imatinib-induced apoptosis of Bcr–Abl-positive human leukaemia cells by enhancing the activation of mitochondria-dependent caspase cascades | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Yonsei Biomedical Research Center (연세의생명연구원) | - |
dc.contributor.googleauthor | Seung Tae Lee | - |
dc.contributor.googleauthor | Jin Seok Kim | - |
dc.contributor.googleauthor | Yoo Hong Min | - |
dc.contributor.googleauthor | Yun Woong Ko | - |
dc.contributor.googleauthor | Jee Sook Hahn | - |
dc.contributor.googleauthor | Hoyoung Maeng | - |
dc.contributor.googleauthor | June-Won Cheong | - |
dc.contributor.googleauthor | Hoi Kyung Jeung | - |
dc.identifier.doi | 10.1046/j.1365-2141.2003.04759.x | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.relation.journalcode | J00409 | - |
dc.identifier.eissn | 1365-2141 | - |
dc.identifier.pmid | 14687026 | - |
dc.identifier.url | http://onlinelibrary.wiley.com/doi/10.1046/j.1365-2141.2003.04759.x/abstract | - |
dc.subject.keyword | imatinib | - |
dc.subject.keyword | apicidin | - |
dc.subject.keyword | histone deacetylase inhibitor | - |
dc.subject.keyword | Bcr–Abl | - |
dc.subject.keyword | leukaemia | - |
dc.contributor.alternativeName | Hahn, Jee Sook | - |
dc.contributor.alternativeName | Ko, Yun Woong | - |
dc.contributor.alternativeName | Kim, Jin Seok | - |
dc.contributor.alternativeName | Maeng, Ho Young | - |
dc.contributor.alternativeName | Min, Yoo Hong | - |
dc.contributor.alternativeName | Lee, Seung Tae | - |
dc.contributor.alternativeName | Cheong, June Won | - |
dc.contributor.alternativeName | Jeung, Hoi Kyung | - |
dc.rights.accessRights | not free | - |
dc.citation.volume | 124 | - |
dc.citation.number | 2 | - |
dc.citation.startPage | 166 | - |
dc.citation.endPage | 178 | - |
dc.identifier.bibliographicCitation | BRITISH JOURNAL OF HAEMATOLOGY, Vol.124(2) : 166-178, 2004 | - |
dc.identifier.rimsid | 35985 | - |
dc.type.rims | ART | - |
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