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Notch1 destabilizes the adherens junction complex through upregulation of the Snail family of E-cadherin repressors in non-small cell lung cancer

DC FieldValueLanguage
dc.contributor.author김세규-
dc.contributor.author김은영-
dc.contributor.author김형중-
dc.contributor.author장윤수-
dc.contributor.author장준-
dc.contributor.author안철민-
dc.date.accessioned2014-12-18T08:58:08Z-
dc.date.available2014-12-18T08:58:08Z-
dc.date.issued2013-
dc.identifier.issn1021-335X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/87288-
dc.description.abstractOne of the critical steps driving cancer cell migration and metastasis is the repression of cell adhesion molecules resulting in loss of cell‑to-cell adhesion. Although interactions between Notch1 and components of the adherens junction complex have been suggested, little is known concerning the consequence of their interactions. In this study, we investigated the interaction between the Notch1 and the E‑cadherin/β‑catenin complex, its effect on the expression of adherens junction complex components and its influence on non-small cell lung cancer (NSCLC) cell proliferation. With progression of lung neoplastic lesions in LSL K-ras G12D mice, the expression of E‑cadherin was inhibited whereas that of Notch1 was increased with frequent nuclear localization, suggesting an inverse relationship between E‑cadherin and Notch1 expression with tumor progression. Transduction of the human Notch1 intracellular domain (N1ICD) into NSCLC cells inhibited expression of E‑cadherin and β‑catenin and induced changes in the localization of adherens junction molecules. The loss of E‑cadherin was mediated through upregulation of the Snail family of transcription factors, Snail and Slug. Experiments in which siRNA against E-cadherin was introduced into NSCLC cells revealed that N1ICD decreased the expression of β‑catenin in an E‑cadherin‑independent manner, leading to inhibition of markers of Wnt/β‑catenin signaling activation. Despite inhibition of Wnt/β‑catenin signaling in the N1ICD‑transduced cells, cells transduced with N1ICD showed no difference in cell cycle progression when compared with that of the control vector-transduced cells. In conclusion, Notch1 inhibited the expression of E‑cadherin through upregulation of the Snail family of transcriptional factors, resulting in inhibition of expression of β‑catenin and destabilization of adherens junctions.-
dc.description.statementOfResponsibilityopen-
dc.relation.isPartOfONCOLOGY REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAdherens Junctions/genetics-
dc.subject.MESHAdherens Junctions/metabolism*-
dc.subject.MESHAdherens Junctions/pathology-
dc.subject.MESHAnimals-
dc.subject.MESHBlotting, Western-
dc.subject.MESHCadherins/genetics-
dc.subject.MESHCadherins/metabolism*-
dc.subject.MESHCarcinoma, Non-Small-Cell Lung/genetics-
dc.subject.MESHCarcinoma, Non-Small-Cell Lung/metabolism*-
dc.subject.MESHCarcinoma, Non-Small-Cell Lung/pathology-
dc.subject.MESHCell Adhesion-
dc.subject.MESHCell Cycle-
dc.subject.MESHCell Proliferation-
dc.subject.MESHHumans-
dc.subject.MESHImmunoenzyme Techniques-
dc.subject.MESHLung Neoplasms/genetics-
dc.subject.MESHLung Neoplasms/metabolism*-
dc.subject.MESHLung Neoplasms/pathology-
dc.subject.MESHMice-
dc.subject.MESHRNA, Messenger/genetics-
dc.subject.MESHReal-Time Polymerase Chain Reaction-
dc.subject.MESHReceptor, Notch1/genetics-
dc.subject.MESHReceptor, Notch1/metabolism*-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHSnail Family Transcription Factors-
dc.subject.MESHTranscription Factors/genetics-
dc.subject.MESHTranscription Factors/metabolism*-
dc.subject.MESHTumor Cells, Cultured-
dc.subject.MESHWnt Proteins/genetics-
dc.subject.MESHWnt Proteins/metabolism*-
dc.subject.MESHbeta Catenin/genetics-
dc.subject.MESHbeta Catenin/metabolism-
dc.titleNotch1 destabilizes the adherens junction complex through upregulation of the Snail family of E-cadherin repressors in non-small cell lung cancer-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Internal Medicine (내과학)-
dc.contributor.googleauthorArum Kim-
dc.contributor.googleauthorEun Young Kim-
dc.contributor.googleauthorEun Na Cho-
dc.contributor.googleauthorHyung Jung Kim-
dc.contributor.googleauthorSe Kyu Kim-
dc.contributor.googleauthorJoon Chang-
dc.contributor.googleauthorChul Min Ahn-
dc.contributor.googleauthorYoon Soo Chang-
dc.identifier.doi10.3892/or.2013.2565-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA00602-
dc.contributor.localIdA01158-
dc.contributor.localIdA02269-
dc.contributor.localIdA03456-
dc.contributor.localIdA03472-
dc.contributor.localIdA00811-
dc.relation.journalcodeJ02419-
dc.identifier.eissn1791-2431-
dc.identifier.pmid23807483-
dc.identifier.urlhttp://www.spandidos-publications.com/or/30/3/1423-
dc.subject.keywordAdherens Junctions/genetics-
dc.subject.keywordAdherens Junctions/metabolism*-
dc.subject.keywordAdherens Junctions/pathology-
dc.subject.keywordAnimals-
dc.subject.keywordBlotting, Western-
dc.subject.keywordCadherins/genetics-
dc.subject.keywordCadherins/metabolism*-
dc.subject.keywordCarcinoma, Non-Small-Cell Lung/genetics-
dc.subject.keywordCarcinoma, Non-Small-Cell Lung/metabolism*-
dc.subject.keywordCarcinoma, Non-Small-Cell Lung/pathology-
dc.subject.keywordCell Adhesion-
dc.subject.keywordCell Cycle-
dc.subject.keywordCell Proliferation-
dc.subject.keywordHumans-
dc.subject.keywordImmunoenzyme Techniques-
dc.subject.keywordLung Neoplasms/genetics-
dc.subject.keywordLung Neoplasms/metabolism*-
dc.subject.keywordLung Neoplasms/pathology-
dc.subject.keywordMice-
dc.subject.keywordRNA, Messenger/genetics-
dc.subject.keywordReal-Time Polymerase Chain Reaction-
dc.subject.keywordReceptor, Notch1/genetics-
dc.subject.keywordReceptor, Notch1/metabolism*-
dc.subject.keywordReverse Transcriptase Polymerase Chain Reaction-
dc.subject.keywordSnail Family Transcription Factors-
dc.subject.keywordTranscription Factors/genetics-
dc.subject.keywordTranscription Factors/metabolism*-
dc.subject.keywordTumor Cells, Cultured-
dc.subject.keywordWnt Proteins/genetics-
dc.subject.keywordWnt Proteins/metabolism*-
dc.subject.keywordbeta Catenin/genetics-
dc.subject.keywordbeta Catenin/metabolism-
dc.contributor.alternativeNameKim, Se Kyu-
dc.contributor.alternativeNameKim, Eun Young-
dc.contributor.alternativeNameKim, Hyung Jung-
dc.contributor.alternativeNameAhn, Chul Min-
dc.contributor.alternativeNameChang, Yoon Soo-
dc.contributor.alternativeNameChang, Joon-
dc.contributor.affiliatedAuthorKim, Se Kyu-
dc.contributor.affiliatedAuthorKim, Hyung Jung-
dc.contributor.affiliatedAuthorAhn, Chul Min-
dc.contributor.affiliatedAuthorChang, Yoon Soo-
dc.contributor.affiliatedAuthorChang, Joon-
dc.contributor.affiliatedAuthorKim, Eun Young-
dc.rights.accessRightsnot free-
dc.citation.volume30-
dc.citation.number3-
dc.citation.startPage1423-
dc.citation.endPage1429-
dc.identifier.bibliographicCitationONCOLOGY REPORTS, Vol.30(3) : 1423-1429, 2013-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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