Biphasic activation of extracellular signal-regulated kinase (ERK) 1/2 in epidermal growth factor (EGF)-stimulated SW480 colorectal cancer cells

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dc.contributor.authorJoo, Donghyunko
dc.contributor.authorWoo, Jong Sooko
dc.contributor.authorCho, Kwang-Hyunko
dc.contributor.authorHan, Seung Hyunko
dc.contributor.authorMin, Tae Sunko
dc.contributor.authorYang Deok Chunko
dc.contributor.authorYun Cheol Heuiko
dc.date.accessioned2016-07-25T09:40:33Z-
dc.date.available2016-07-25T09:40:33Z-
dc.date.created2016-06-20-
dc.date.created2016-06-20-
dc.date.issued2016-04-
dc.identifier.citationBMB REPORTS, v.49, no.4, pp.220 - 225-
dc.identifier.issn1976-6696-
dc.identifier.urihttp://hdl.handle.net/10203/212162-
dc.description.abstractCancer cells have different characteristics due to the genetic differences where these unique features may strongly influence the effectiveness of therapeutic interventions. Here, we show that the spontaneous reactivation of extracellular signal-regulated kinase (ERK), distinct from conventional ERK activation, represents a potent mechanism for cancer cell survival. We studied ERK1/2 activation in vitro in SW480 colorectal cancer cells. Although ERK signaling tends to be transiently activated, we observed the delayed reactivation of ERK1/2 in epidermal growth factor (EGF)-stimulated SW480 cells. This effect was observed even after EGF withdrawal. While phosphorylated ERK1/2 translocated into the nucleus following its primary activation, it remained in the cytoplasm during late-phase activation. The inhibition of primary ERK1/2 activation or protein trafficking, blocked reactivation and concurrently increased caspase 3 activity. Our results suggest that the biphasic activation of ERK1/2 plays a role in cancer cell survival; thus, regulation of ERK1/2 activation may improve the efficacy of cancer therapies that target ERK signaling.-
dc.languageEnglish-
dc.publisherKOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY-
dc.subject2 DISTINCT PHASES-
dc.subjectPROTEIN-KINASE-
dc.subjectSUSTAINED ACTIVATION-
dc.subjectMAP KINASES-
dc.subjectEXPRESSION-
dc.subjectPATHWAYS-
dc.subjectPROLIFERATION-
dc.subjectCASCADE-
dc.titleBiphasic activation of extracellular signal-regulated kinase (ERK) 1/2 in epidermal growth factor (EGF)-stimulated SW480 colorectal cancer cells-
dc.typeArticle-
dc.identifier.wosid000378131700006-
dc.identifier.scopusid2-s2.0-84966671398-
dc.type.rimsART-
dc.citation.volume49-
dc.citation.issue4-
dc.citation.beginningpage220-
dc.citation.endingpage225-
dc.citation.publicationnameBMB REPORTS-
dc.identifier.doi10.5483/BMBRep.2016.49.4.004-
dc.contributor.localauthorCho, Kwang-Hyun-
dc.contributor.nonIdAuthorJoo, Donghyun-
dc.contributor.nonIdAuthorWoo, Jong Soo-
dc.contributor.nonIdAuthorHan, Seung Hyun-
dc.contributor.nonIdAuthorMin, Tae Sun-
dc.contributor.nonIdAuthorYang Deok Chun-
dc.contributor.nonIdAuthorYun Cheol Heui-
dc.description.isOpenAccessY-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorBiphasic activation-
dc.subject.keywordAuthorCancer cell survival-
dc.subject.keywordAuthorERK pathway-
dc.subject.keywordAuthorpERK translocation-
dc.subject.keywordAuthorSW480 cells-
dc.subject.keywordPlus2 DISTINCT PHASES-
dc.subject.keywordPlusPROTEIN-KINASE-
dc.subject.keywordPlusSUSTAINED ACTIVATION-
dc.subject.keywordPlusMAP KINASES-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusPATHWAYS-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusCASCADE-
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BiS-Journal Papers(저널논문)
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