TWEAK/Fn14 signaling mediates gastric cancer cell resistance to 5-fluorouracil via NF-kB activation

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dc.contributor.authorOh Hyung Kwon-
dc.contributor.authorJong Hwan Kim-
dc.contributor.authorSeon-Young Kim-
dc.contributor.authorYong Sung Kim-
dc.date.accessioned2017-04-19T09:48:04Z-
dc.date.available2017-04-19T09:48:04Z-
dc.date.issued2014-
dc.identifier.issn1019-6439-
dc.identifier.uri10.3892/ijo.2013.2211ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11739-
dc.description.abstractChemoresistance is one of the most serious problems in the treatment of cancer. In the present study, we show that Fn14 promotes resistance to 5-fluorouracil (5-FU) in gastric cancer (GC). We found that 5-FU treatment upregulated Fn14 expression in various cancer cell lines, including GC cell lines, and that knockdown of Fn14 using shRNA accelerated 5-FU sensitivity. In contrast, Fn14 overexpression or TWEAK treatment promoted resistance to 5-FU. Furthermore, we investigated the mechanisms underlying Fn14-mediated chemoresistance. We first revealed that 5-FU-mediated upregulation of Fn14 occurred as a result of NF-κB activation, indicating that 5-FU-mediated NF-κB activation was the principal event underlying Fn14 upregulation and 5-FU resistance in GC. Taken together, our results suggest that Fn14 is a novel therapeutic target and that inhibition of Fn14 combined with 5-FU treatment may be an effective molecular therapeutic strategy to treat 5-FU-resistant gastric cancers-
dc.publisherSpandidos Publ Ltd-
dc.titleTWEAK/Fn14 signaling mediates gastric cancer cell resistance to 5-fluorouracil via NF-kB activation-
dc.title.alternativeTWEAK/Fn14 signaling mediates gastric cancer cell resistance to 5-fluorouracil via NF-kB activation-
dc.typeArticle-
dc.citation.titleInternational Journal of Oncology-
dc.citation.number2-
dc.citation.endPage590-
dc.citation.startPage583-
dc.citation.volume44-
dc.contributor.affiliatedAuthorOh Hyung Kwon-
dc.contributor.affiliatedAuthorJong Hwan Kim-
dc.contributor.affiliatedAuthorSeon-Young Kim-
dc.contributor.affiliatedAuthorYong Sung Kim-
dc.contributor.alternativeName권오형-
dc.contributor.alternativeName김종환-
dc.contributor.alternativeName김선영-
dc.contributor.alternativeName김용성-
dc.identifier.bibliographicCitationInternational Journal of Oncology, vol. 44, no. 2, pp. 583-590-
dc.identifier.doi10.3892/ijo.2013.2211-
dc.subject.keywordchemoresistance-
dc.subject.keyword5-FU-
dc.subject.keywordgastric cancer-
dc.subject.keywordNF-κB-
dc.subject.keywordFn14-
dc.subject.localchemoresistance-
dc.subject.localChemoresistance-
dc.subject.localChemo-resistance-
dc.subject.local5-FU-
dc.subject.localgastric cancer-
dc.subject.localGastric cancer (GC)-
dc.subject.localGastric cancer-
dc.subject.localNuclear factor-kappa B-
dc.subject.localnuclear factor κB-
dc.subject.localNf-κb-
dc.subject.localNF-kB-
dc.subject.localnuclear factor kappa B-
dc.subject.localNF-κB (nuclear factor kappa-B)-
dc.subject.localNF-kappaB-
dc.subject.localNuclear factor-κb-
dc.subject.localNF-κ B-
dc.subject.localNF-κB-
dc.subject.localNF-kappa B-
dc.subject.localNuclear factor κB (NF-κB)-
dc.subject.localNuclear factor κB-
dc.subject.localNFκB-
dc.subject.localNf-κB-
dc.subject.localNuclear factor-κB-
dc.subject.localnuclear factorκB-
dc.subject.localNuclear factor (NF)-κB-
dc.subject.localNuclear factor kappa B-
dc.subject.localnuclear factor-κB-
dc.subject.localNF-ΚB-
dc.subject.localNuclear factor-kappa B (NF-κB)-
dc.subject.localNuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB-
dc.subject.localnuclear factor-kappaB (NF-κB)-
dc.subject.localNFkappaB-
dc.subject.localNuclear factor kappaB-
dc.subject.localFn14-
dc.description.journalClassY-
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