Cited 0 times in
Two distinct modes of cell death induced by doxorubicin: apoptosis and cell death through mitotic catastrophe accompanied by senescence-like phenotype.
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Eom, YW | - |
dc.contributor.author | Kim, MA | - |
dc.contributor.author | Park, SS | - |
dc.contributor.author | Goo, MJ | - |
dc.contributor.author | Kwon, HJ | - |
dc.contributor.author | Sohn, S | - |
dc.contributor.author | Kim, WH | - |
dc.contributor.author | Yoon, G | - |
dc.contributor.author | Choi, KS | - |
dc.date.accessioned | 2011-07-05T04:55:44Z | - |
dc.date.available | 2011-07-05T04:55:44Z | - |
dc.date.issued | 2005 | - |
dc.identifier.issn | 0950-9232 | - |
dc.identifier.uri | http://repository.ajou.ac.kr/handle/201003/3239 | - |
dc.description.abstract | Chronic exposure of many human hepatoma cell lines to a low dose (LD) of doxorubicin induced a senescence-like phenotype (SLP) accompanied by enlargement of cells and increased senescence-associated beta-galactosidase activity. LD doxorubicin-induced SLP was preceded by multinucleation and downregulation of multiple proteins with mitotic checkpoint function, including CENP-A, Mad2, BubR1, and Chk1. LD doxorubicin-treated cells eventually underwent cell death through mitotic catastrophe. When we investigated whether LD doxorubicin-induced cell death shares biochemical characteristics with high dose (HD) doxorubicin-induced apoptosis in Huh-7 cells, we observed that externalization of phosphatidyl serine and release of mitochondrial cytochrome c into the cytosol was associated with both types of cell death. However, propidium iodide exclusion assays showed that membrane integrity was lost in the initial phase of LD doxorubicin-induced cell death through mitotic catastrophe, whereas it was lost during the late phase of HD doxorubicin-induced apoptosis. Furthermore, HD doxorubicin-induced apoptosis but not LD doxorubicin-induced mitotic catastrophe led to transient activation of NF-kappaB and strong, sustained activations of p38, c-Jun N-terminal kinase, and caspases. Collectively, these results indicate that different doses of doxorubicin activate different regulatory mechanisms to induce either apoptosis or cell death through mitotic catastrophe. | - |
dc.language.iso | en | - |
dc.subject.MESH | Apoptosis | - |
dc.subject.MESH | Caspases | - |
dc.subject.MESH | Cell Aging | - |
dc.subject.MESH | Cell Death | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Cell Membrane Permeability | - |
dc.subject.MESH | Cell Nucleus | - |
dc.subject.MESH | Cytochromes c | - |
dc.subject.MESH | DNA | - |
dc.subject.MESH | Down-Regulation | - |
dc.subject.MESH | Doxorubicin | - |
dc.subject.MESH | Enzyme Activation | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Kinetics | - |
dc.subject.MESH | Lamin Type B | - |
dc.subject.MESH | Microscopy, Electron, Transmission | - |
dc.subject.MESH | Mitochondria | - |
dc.subject.MESH | Mitosis | - |
dc.subject.MESH | Mitotic Spindle Apparatus | - |
dc.subject.MESH | Models, Biological | - |
dc.subject.MESH | NF-kappa B | - |
dc.subject.MESH | Phenotype | - |
dc.subject.MESH | Signal Transduction | - |
dc.subject.MESH | p38 Mitogen-Activated Protein Kinases | - |
dc.title | Two distinct modes of cell death induced by doxorubicin: apoptosis and cell death through mitotic catastrophe accompanied by senescence-like phenotype. | - |
dc.type | Article | - |
dc.identifier.pmid | 15870702 | - |
dc.contributor.affiliatedAuthor | 손, 성향 | - |
dc.contributor.affiliatedAuthor | 김, 욱환 | - |
dc.contributor.affiliatedAuthor | 윤, 계순 | - |
dc.contributor.affiliatedAuthor | 최, 경숙 | - |
dc.type.local | Journal Papers | - |
dc.identifier.doi | 10.1038/sj.onc.1208627 | - |
dc.citation.title | Oncogene | - |
dc.citation.volume | 24 | - |
dc.citation.number | 30 | - |
dc.citation.date | 2005 | - |
dc.citation.startPage | 4765 | - |
dc.citation.endPage | 4777 | - |
dc.identifier.bibliographicCitation | Oncogene, 24(30). : 4765-4777, 2005 | - |
dc.identifier.eissn | 1476-5594 | - |
dc.relation.journalid | J009509232 | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.