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Two distinct modes of cell death induced by doxorubicin: apoptosis and cell death through mitotic catastrophe accompanied by senescence-like phenotype.

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dc.contributor.authorEom, YW-
dc.contributor.authorKim, MA-
dc.contributor.authorPark, SS-
dc.contributor.authorGoo, MJ-
dc.contributor.authorKwon, HJ-
dc.contributor.authorSohn, S-
dc.contributor.authorKim, WH-
dc.contributor.authorYoon, G-
dc.contributor.authorChoi, KS-
dc.date.accessioned2011-07-05T04:55:44Z-
dc.date.available2011-07-05T04:55:44Z-
dc.date.issued2005-
dc.identifier.issn0950-9232-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/3239-
dc.description.abstractChronic 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.isoen-
dc.subject.MESHApoptosis-
dc.subject.MESHCaspases-
dc.subject.MESHCell Aging-
dc.subject.MESHCell Death-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHCell Membrane Permeability-
dc.subject.MESHCell Nucleus-
dc.subject.MESHCytochromes c-
dc.subject.MESHDNA-
dc.subject.MESHDown-Regulation-
dc.subject.MESHDoxorubicin-
dc.subject.MESHEnzyme Activation-
dc.subject.MESHHumans-
dc.subject.MESHKinetics-
dc.subject.MESHLamin Type B-
dc.subject.MESHMicroscopy, Electron, Transmission-
dc.subject.MESHMitochondria-
dc.subject.MESHMitosis-
dc.subject.MESHMitotic Spindle Apparatus-
dc.subject.MESHModels, Biological-
dc.subject.MESHNF-kappa B-
dc.subject.MESHPhenotype-
dc.subject.MESHSignal Transduction-
dc.subject.MESHp38 Mitogen-Activated Protein Kinases-
dc.titleTwo distinct modes of cell death induced by doxorubicin: apoptosis and cell death through mitotic catastrophe accompanied by senescence-like phenotype.-
dc.typeArticle-
dc.identifier.pmid15870702-
dc.contributor.affiliatedAuthor손, 성향-
dc.contributor.affiliatedAuthor김, 욱환-
dc.contributor.affiliatedAuthor윤, 계순-
dc.contributor.affiliatedAuthor최, 경숙-
dc.type.localJournal Papers-
dc.identifier.doi10.1038/sj.onc.1208627-
dc.citation.titleOncogene-
dc.citation.volume24-
dc.citation.number30-
dc.citation.date2005-
dc.citation.startPage4765-
dc.citation.endPage4777-
dc.identifier.bibliographicCitationOncogene, 24(30). : 4765-4777, 2005-
dc.identifier.eissn1476-5594-
dc.relation.journalidJ009509232-
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Microbiology
Journal Papers > School of Medicine / Graduate School of Medicine > Surgery
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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