Polyamine depletion partially reduces the radiation-induced cell death via cell cycle delay mediated by thioredoxin

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dc.contributor.authorM S Moon-
dc.contributor.authorJ S Kim-
dc.contributor.authorT L Kim-
dc.contributor.authorJ J Yum-
dc.contributor.authorEun Wie Cho-
dc.contributor.authorI G Kim-
dc.date.accessioned2017-04-19T09:06:22Z-
dc.date.available2017-04-19T09:06:22Z-
dc.date.issued2006-
dc.identifier.issn0742-2091-
dc.identifier.uri10.1007/s10565-006-0042-zko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7752-
dc.description.abstractIn previous studies, polyamine depletion by DFMO (α- difluoromethylornithine)-treatment reduced H2O2-induced apoptotic cell death by reduction of ferric ion uptake. In the present study, we analyzed the reduction of radiation-induced cell death by polyamine depletion. Exposure of HT29 cells to radiation induced severe cell death, but when cells were pretreated with DFMO, a specific inhibitor of polyamine biosynthesis, radiation-induced cell death was reduced to 50-60% of control. Cell cycle analysis showed that, in these cells, the time to reach the G2/M phase arrest was delayed for 20-24 h compared to the control cells, at which stage the fate of cells exposed to ionizing radiation is determined. DFMO-treated cells also showed a low level of thioredoxin, which is a high-level determinant of the cellular fate. To investigate the relationship between the G2/M phase arrest and the reduction of thioredoxin caused by polyamine depletion, we also analyzed thioredoxin-antisensed (asTRX) HT29 cells as for DFMO-treated cells. In asTRX-transfected cells, the γ-irradiation- induced G2/M phase arrest was also significantly delayed and radiation-induced cell death was profoundly reduced, as in the DFMO-treated cells. Both sets of cells showed a decrease of cyclin D1 and an increment of HSP25, which are involved in radiation-induced cell cycle progress. Overall, these results suggest that polyamines are essential for normal cell death of HT29 cells triggered by γ-radiation and that this is partially mediated by the regulation of thioredoxin expression.-
dc.publisherSpringer-
dc.titlePolyamine depletion partially reduces the radiation-induced cell death via cell cycle delay mediated by thioredoxin-
dc.title.alternativePolyamine depletion partially reduces the radiation-induced cell death via cell cycle delay mediated by thioredoxin-
dc.typeArticle-
dc.citation.titleCell Biology and Toxicology-
dc.citation.number2-
dc.citation.endPage147-
dc.citation.startPage137-
dc.citation.volume22-
dc.contributor.affiliatedAuthorEun Wie Cho-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName-
dc.contributor.alternativeName조은위-
dc.contributor.alternativeName-
dc.identifier.bibliographicCitationCell Biology and Toxicology, vol. 22, no. 2, pp. 137-147-
dc.identifier.doi10.1007/s10565-006-0042-z-
dc.subject.keywordCell cycle delay-
dc.subject.keywordCyclin D1-
dc.subject.keywordDFMO-
dc.subject.keywordHSP25-
dc.subject.keywordPolyamine-
dc.subject.keywordRadiation-induced cell death-
dc.subject.keywordThioredoxin-
dc.subject.localCell cycle delay-
dc.subject.localcyclin D1-
dc.subject.localCyclin D1-
dc.subject.localDFMO-
dc.subject.localHSP25-
dc.subject.localpolyamine-
dc.subject.localPolyamine-
dc.subject.localRadiation-induced cell death-
dc.subject.localthioredoxin-
dc.subject.localThioredoxin-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
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