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PEROXIREDOXIN IV PROTECTS CELLS FROM RADIATION-INDUCED APOPTOSIS IN HEAD-AND-NECK SQUAMOUS CELL CARCINOMA

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dc.contributor.authorPark, Jung Je-
dc.contributor.authorChang, Hyo Won-
dc.contributor.authorJeong, Eun-Jeong-
dc.contributor.authorRoh, Jong-Lyel-
dc.contributor.authorChoi, Seung-Ho-
dc.contributor.authorJeon, Sea-Yuong-
dc.contributor.authorKo, Gyung Hyuck-
dc.contributor.authorKim, Sang Yoon-
dc.date.accessioned2022-12-27T05:19:06Z-
dc.date.available2022-12-27T05:19:06Z-
dc.date.issued2009-03-15-
dc.identifier.issn0360-3016-
dc.identifier.issn1879-355X-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/26365-
dc.description.abstractPurpose: Human peroxiredoxins (Prxs) are known as a family of thiol-specific antioxidant enzymes, among which Prx-I and -II play an important role in protecting cells from irradiation-induced cell death. It is not known whether Prx-IV also protects cells from ionizing radiation (IR). Methods and Materials: To evaluate the protective role of Prx-IV in IR, we transfected full-length Prx-IV cDNA into AMC-HN3 cells, which weakly express endogenous Prx-IV, and knocked down the expression of Prx-IV with siRNA methods using AMC-HN7 cells, which express high levels of endogenous Prx-IV. Radiosensitivity profiles in these cells were evaluated using clonogenic assay, FACS analysis, cell viability, and TUNEL assay. Results: Three Prx-IV expressing clones were isolated. Prx-IV regulated intracellular reactive oxygen species (ROS) levels and made cells more resistant to IR-induced apoptosis. Furthermore, the knockdown of Prx-IV with siRNA made cells more sensitive to IR-induced apoptosis. Conclusion: The results of these studies suggest that Prx-IV may play an important role in protecting cells from IR-induced apoptosis in head-and-neck squamous cell carcinoma. (C) 2009 Elsevier Inc.-
dc.format.extent7-
dc.language영어-
dc.language.isoENG-
dc.publisherELSEVIER SCIENCE INC-
dc.titlePEROXIREDOXIN IV PROTECTS CELLS FROM RADIATION-INDUCED APOPTOSIS IN HEAD-AND-NECK SQUAMOUS CELL CARCINOMA-
dc.typeArticle-
dc.publisher.location미국-
dc.identifier.doi10.1016/j.ijrobp.2008.10.070-
dc.identifier.wosid000264257400035-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS, v.73, no.4, pp 1196 - 1202-
dc.citation.titleINTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS-
dc.citation.volume73-
dc.citation.number4-
dc.citation.startPage1196-
dc.citation.endPage1202-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalResearchAreaRadiology, Nuclear Medicine & Medical Imaging-
dc.relation.journalWebOfScienceCategoryOncology-
dc.relation.journalWebOfScienceCategoryRadiology, Nuclear Medicine & Medical Imaging-
dc.subject.keywordPlusMANGANESE SUPEROXIDE-DISMUTASE-
dc.subject.keywordPlusTHIOREDOXIN PEROXIDASE-
dc.subject.keywordPlusIONIZING-RADIATION-
dc.subject.keywordPlusREACTIVE OXYGEN-
dc.subject.keywordPlusANTIOXIDANT DEFENSE-
dc.subject.keywordPlusOXIDATIVE STRESS-
dc.subject.keywordPlusGENE-EXPRESSION-
dc.subject.keywordPlusCANCER CELLS-
dc.subject.keywordPlusTUMOR-GROWTH-
dc.subject.keywordPlusLUNG-CANCER-
dc.subject.keywordAuthorPeroxiredoxin IV-
dc.subject.keywordAuthorRadiation seisitivity-
dc.subject.keywordAuthorApoptosis-
dc.subject.keywordAuthorReactive oxygen species-
dc.subject.keywordAuthorHead-and-neck cancer-
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