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Upregulation and secretion of macrophage inhibitory cytokine-1 (MIC-1) in gastric cancers

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dc.contributor.authorBaek, Kyoung Eun-
dc.contributor.authorYoon, Suk Ran-
dc.contributor.authorKim, Jong-Tae-
dc.contributor.authorKim, Kwang Soo-
dc.contributor.authorKang, Seong Ho-
dc.contributor.authorYang, Young-
dc.contributor.authorLim, Jong-Seok-
dc.contributor.authorChoi, Inpyo-
dc.contributor.authorNam, Myoung Soo-
dc.contributor.authorYoon, Michung-
dc.contributor.authorLee, Hee Gu-
dc.date.available2021-02-22T14:18:00Z-
dc.date.created2020-09-03-
dc.date.issued2009-03-
dc.identifier.issn0009-8981-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13812-
dc.description.abstractBackground: Macrophage inhibitory cytokine-1 (MIC-1), a distant member of the transforming growth factor (TGF)-beta superfamily, has been reported to be upregulated and secreted from several cancers. We examined MIC-1 expression and secretion in gastric cancers. Methods: MIC-I mRNA and protein levels in cancer tissues and cell lines were analyzed by RT-PCR and Western blot. MIC-1 expression in cancer tissues and its secretion in serum were analyzed using immunohistochemistry and ELISA. Results: MIC-I was significantly upregulated in gastric cancer tissues and cell lines. MIC-1 was secreted from gastric SNU620 cells and its levels in the serum of cancer patients were 10-fold higher than those of healthy controls. In addition, the staining of MIC-I expression was strongly increased in metastatic gastric cancers. Conclusions: MIC-I was obviously overexpressed in gastric cancers and MICA secretion into blood may be useful for the prediction of gastric cancer progression. Crown Copyright (C) 2008 Published by Elsevier B.V. All rights reserved.-
dc.language영어-
dc.language.isoen-
dc.publisherELSEVIER SCIENCE BV-
dc.titleUpregulation and secretion of macrophage inhibitory cytokine-1 (MIC-1) in gastric cancers-
dc.typeArticle-
dc.contributor.affiliatedAuthorYang, Young-
dc.contributor.affiliatedAuthorLim, Jong-Seok-
dc.identifier.doi10.1016/j.cca.2008.12.008-
dc.identifier.scopusid2-s2.0-58549108814-
dc.identifier.wosid000263797000026-
dc.identifier.bibliographicCitationCLINICA CHIMICA ACTA, v.401, no.1-2, pp.128 - 133-
dc.relation.isPartOfCLINICA CHIMICA ACTA-
dc.citation.titleCLINICA CHIMICA ACTA-
dc.citation.volume401-
dc.citation.number1-2-
dc.citation.startPage128-
dc.citation.endPage133-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaMedical Laboratory Technology-
dc.relation.journalWebOfScienceCategoryMedical Laboratory Technology-
dc.subject.keywordPlusTGF-BETA SUPERFAMILY-
dc.subject.keywordPlusGROWTH-FACTOR-BETA-
dc.subject.keywordPlusPROSTATE-CANCER-
dc.subject.keywordPlusMORPHOGENETIC PROTEIN-
dc.subject.keywordPlusMEMBER-
dc.subject.keywordPlusCELLS-
dc.subject.keywordPlusP53-
dc.subject.keywordPlusSERUM-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordAuthorMIC-1-
dc.subject.keywordAuthorMacrophage-inhibitory cytokine-1-
dc.subject.keywordAuthorGDF-15-
dc.subject.keywordAuthorGrowth differentiation factor-15-
dc.subject.keywordAuthorGastric cancer-
dc.identifier.urlhttps://www.sciencedirect.com/science/article/abs/pii/S0009898108005883?via%3Dihub-
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