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Romo1 and the NF-kappa B pathway are involved in oxidative stress-induced tumor cell invasion

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dc.contributor.authorLee, Sora-
dc.contributor.authorPark, Yoon Hee-
dc.contributor.authorChung, Jin Sil-
dc.contributor.authorYoo, Young Do-
dc.date.accessioned2021-09-04T16:49:00Z-
dc.date.available2021-09-04T16:49:00Z-
dc.date.created2021-06-18-
dc.date.issued2015-05-
dc.identifier.issn1019-6439-
dc.identifier.urihttps://scholar.korea.ac.kr/handle/2021.sw.korea/93746-
dc.description.abstractReactive oxygen species (ROS) are important contributors to tumor cell invasion. ROS enhanced by reactive oxygen species modulator 1 (Romol) expression has been reported to increase invasive potential and constitutive activation of nuclear factor-kappa B (NF-kappa B) in hepatocellular carcinoma (HCC). Therefore, we investigated whether constitutive NF-kappa B activation due to Romol expression is associated with breast cancer tumor cell invasion. In this study, we show that oxidative stress-induced invasion is mediated by Romol expression. The Romol-induced increase of invasive activity was blocked by an inhibitor of kappa B kinase (IKK). These tesults demonstrate that tumor cell invasion in response to oxidative stress is associated with Romol expression and the NF-kappa B signaling pathway. Romol is therefore a promising therapeutic target for diseases characterized by NF-kappa B deregulation.-
dc.languageEnglish-
dc.language.isoen-
dc.publisherSPANDIDOS PUBL LTD-
dc.subjectOXYGEN SPECIES PRODUCTION-
dc.subjectTRANSCRIPTION FACTOR-
dc.subjectHYDROGEN-PEROXIDE-
dc.subjectEPITHELIAL-CELLS-
dc.subjectROS PRODUCTION-
dc.subjectACTIVATION-
dc.subjectCANCER-
dc.subjectEXPRESSION-
dc.subjectCARCINOMA-
dc.subjectIKK-
dc.titleRomo1 and the NF-kappa B pathway are involved in oxidative stress-induced tumor cell invasion-
dc.typeArticle-
dc.contributor.affiliatedAuthorYoo, Young Do-
dc.identifier.doi10.3892/ijo.2015.2889-
dc.identifier.scopusid2-s2.0-84925436766-
dc.identifier.wosid000353180800018-
dc.identifier.bibliographicCitationINTERNATIONAL JOURNAL OF ONCOLOGY, v.46, no.5, pp.2021 - 2028-
dc.relation.isPartOfINTERNATIONAL JOURNAL OF ONCOLOGY-
dc.citation.titleINTERNATIONAL JOURNAL OF ONCOLOGY-
dc.citation.volume46-
dc.citation.number5-
dc.citation.startPage2021-
dc.citation.endPage2028-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.subject.keywordPlusOXYGEN SPECIES PRODUCTION-
dc.subject.keywordPlusTRANSCRIPTION FACTOR-
dc.subject.keywordPlusHYDROGEN-PEROXIDE-
dc.subject.keywordPlusEPITHELIAL-CELLS-
dc.subject.keywordPlusROS PRODUCTION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusCARCINOMA-
dc.subject.keywordPlusIKK-
dc.subject.keywordAuthorreactive oxygen species-
dc.subject.keywordAuthornuclear factor-kappa B-
dc.subject.keywordAuthortumor invasion-
dc.subject.keywordAuthorRomo1-
dc.subject.keywordAuthoroxidative stress-
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