Mitomycin C modulates DNA-double strand break repair genes in cervical carcinoma cells

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dc.contributor.authorYun Hee Kang-
dc.contributor.authorK A Lee-
dc.contributor.authorJ H Kim-
dc.contributor.authorSung Goo Park-
dc.contributor.authorD Y Yoon-
dc.date.accessioned2017-04-19T09:20:01Z-
dc.date.available2017-04-19T09:20:01Z-
dc.date.issued2010-
dc.identifier.issn0939-4451-
dc.identifier.uri10.1007/s00726-010-0568-5ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/9807-
dc.description.abstractIn a previous study, we elucidated the apoptotic mechanism mediated via Fas/FasL-dependent pathway in mitomycin C-treated cervical carcinoma cells. In this study, 2-D and MALDI-TOF analyses were performed in order to search mitomycin C-induced modulators in cervical carcinoma cells. Some protein spots down- or up-regulated by mitomycin C were separately selected from the 2-D gels. Twenty protein spots were identified from the 2-D gels. Among the 20 spots, 11 spots were down-regulated, whereas 9 spots were up-regulated in SiHa/pRSV-luc cells by mitomycin C. Three spots have not been identified in the database. Ku70-binding protein (KUB3), MHC class I antigen, MHC class I chain-related protein A or multi-PDZ domain protein 1, MAGUK P55 subfamily member 3 or lamda/iota protein kinase C-interacting protein, and GL014 or Sad1/unc-84 protein-like 1 were suppressed by mitomycin C treatment. Heat shock 60 kDa protein 1 (chaperonin), similar to heat shock protein 90 kDa protein alpha or ninein centrosomal protein isoform C, NADP-dependent malic enzyme, mitochondrial precursor, GRB10 adaptor protein, glycogenin-interacting protein 1, cystathionine gamma-lyase, G2/mitotic-specific cyclin B2 or heat shock 90 kDa protein 1 alpha, peptidyl-prolyl cis-trans isomerase B, and PARP-2 (fragment) were induced by mitomycin C. KUB3, Brca1, and E6 gene expressions were down-regulated by mitomycin C in HPV-positive cervical cancer cells, SiHa/pRSV-luc and SiHa. In these studies, we suggest that MMC down-regulated the expression levels of the upstream molecules of DNA-double strand break repair system, non-homologous end joining or homologous recombination, resulting in the suppression of cervical cancer cell growth.-
dc.publisherSpringer-
dc.titleMitomycin C modulates DNA-double strand break repair genes in cervical carcinoma cells-
dc.title.alternativeMitomycin C modulates DNA-double strand break repair genes in cervical carcinoma cells-
dc.typeArticle-
dc.citation.titleAmino Acids-
dc.citation.number5-
dc.citation.endPage1298-
dc.citation.startPage1291-
dc.citation.volume39-
dc.contributor.affiliatedAuthorYun Hee Kang-
dc.contributor.affiliatedAuthorSung Goo Park-
dc.contributor.alternativeName강윤희-
dc.contributor.alternativeName이경애-
dc.contributor.alternativeName김정희-
dc.contributor.alternativeName박성구-
dc.contributor.alternativeName윤도영-
dc.identifier.bibliographicCitationAmino Acids, vol. 39, no. 5, pp. 1291-1298-
dc.identifier.doi10.1007/s00726-010-0568-5-
dc.subject.keywordCervical carcinoma cells-
dc.subject.keywordDSB repair genes-
dc.subject.keywordKu70-binding protein-
dc.subject.keywordMitomycin C-
dc.subject.localCervical carcinoma cells-
dc.subject.localcervical carcinoma cell-
dc.subject.localDSB repair genes-
dc.subject.localKu70-binding protein-
dc.subject.localMitomycin C-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Disease Target Structure Research Center > 1. Journal Articles
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