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Marmesin-mediated suppression of VEGF/VEGFR and integrin beta 1 expression: Its implication in non-small cell lung cancer cell responses and tumor angiogenesis

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dc.contributor.authorKim, Jae Hyeon-
dc.contributor.authorKim, Min Su-
dc.contributor.authorLee, Bo Hee-
dc.contributor.authorKim, Jin-Kyu-
dc.contributor.authorAhn, Eun Kyung-
dc.contributor.authorKo, Hye-Jin-
dc.contributor.authorCho, Young-Rak-
dc.contributor.authorLee, Sang-Jin-
dc.contributor.authorBae, Gyu-Un-
dc.contributor.authorKim, Yong Kee-
dc.contributor.authorOh, Joa Sub-
dc.contributor.authorSeo, Dong-Wan-
dc.date.available2021-02-22T11:17:45Z-
dc.date.issued2017-01-
dc.identifier.issn1021-335X-
dc.identifier.issn1791-2431-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8912-
dc.description.abstractIn the present study, we investigated the effects and molecular mechanism of marmesin, a natural coumarin compound isolated from Broussonetia kazinoki, on non-small cell lung cancer (NSCLC) cell responses and tumor angiogenesis. Marmesin abrogated mitogen-stimulated proliferation and invasion in both p53 wild-type A549 and p53-deficient H1299 NSCLC cells. These antitumor activities of marmesin were mediated by the inactivation of mitogenic signaling pathways and downregulation of cell signaling-related proteins including vascular endothelial growth factor receptor-2 (VEGFR-2), integrin beta 1, integrin-linked kinase and matrix metalloproteinases-2. Furthermore, marmesin suppressed the expression and secretion of VEGF in both NSCLC cells, leading to inhibition of capillary-like structure formation in human umbilical vein endothelial cells. Collectively, these findings demonstrate the pharmacological roles and molecular targets of marmesin in regulating NSCLC cell responses and tumor angiogenesis.-
dc.format.extent7-
dc.language영어-
dc.language.isoENG-
dc.publisherSPANDIDOS PUBL LTD-
dc.titleMarmesin-mediated suppression of VEGF/VEGFR and integrin beta 1 expression: Its implication in non-small cell lung cancer cell responses and tumor angiogenesis-
dc.typeArticle-
dc.publisher.location그리이스-
dc.identifier.doi10.3892/or.2016.5245-
dc.identifier.scopusid2-s2.0-85006434685-
dc.identifier.wosid000390639800011-
dc.identifier.bibliographicCitationONCOLOGY REPORTS, v.37, no.1, pp 91 - 97-
dc.citation.titleONCOLOGY REPORTS-
dc.citation.volume37-
dc.citation.number1-
dc.citation.startPage91-
dc.citation.endPage97-
dc.type.docTypeArticle-
dc.description.isOpenAccessY-
dc.description.journalRegisteredClasssci-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalWebOfScienceCategoryOncology-
dc.subject.keywordPlusBROUSSONETIA-KAZINOKI-
dc.subject.keywordPlusMATRIX METALLOPROTEINASES-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordPlusMECHANISM-
dc.subject.keywordPlusMIGRATION-
dc.subject.keywordPlusMICROENVIRONMENT-
dc.subject.keywordPlusCONSTITUENTS-
dc.subject.keywordPlusINVASION-
dc.subject.keywordPlusDISEASES-
dc.subject.keywordAuthormarmesin-
dc.subject.keywordAuthornon-small cell lung cancer-
dc.subject.keywordAuthorVEGFR-2-
dc.subject.keywordAuthorVEGF-
dc.subject.keywordAuthorintegrin beta 1-
dc.identifier.urlhttps://www.spandidos-publications.com/10.3892/or.2016.5245-
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