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KAI1/CD82 suppresses tumor invasion by MMP9 inactivation via TIMP1 up-regulation in the H1299 human lung carcinoma cell line

DC FieldValueLanguage
dc.contributor.author이운규-
dc.date.accessioned2015-06-10T12:26:06Z-
dc.date.available2015-06-10T12:26:06Z-
dc.date.issued2006-
dc.identifier.issn0006-291X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/109795-
dc.description.abstractWe conducted a study on the mechanism of KAI1/CD82-mediated suppression of tumor invasiveness and metastasis, and examined its effect on MMP-9 activity and the TIMP1 levels in H1299 human non-small cell lung carcinoma cells. The H1299 human lung carcinoma cells were transfected with pcDNA3.1-CD82 and stable transfectant clones that had a high KAI1/CD82 expression were obtained. We performed Western blot analysis, cell invasion assay, gelatin zymography, and RT-PCR to assess the KAI1/CD82 expression and tumor invasiveness, the MMP-9 activity, the MMP-9 mRNA and protein levels, and the TIMP1 levels in the H1299/CD82 transfectant cells and compared the results with those of the control groups. The H1299/CD82 transfectants exhibited significant suppression of cell invasion, reduced MMP9 enzyme activity, elevated MMP9 mRNA and MMP-9 protein levels, and elevated TIMP1 levels. It may be postulated that KAI1/CD82 over-expression in the H1299 non-small cell lung carcinoma cells suppresses the tumor invasiveness and metastatic potential by inducing MMP9 inactivation via the up-regulation of TIMP1.-
dc.description.statementOfResponsibilityopen-
dc.format.extent655~661-
dc.relation.isPartOfBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHCarcinoma/enzymology-
dc.subject.MESHCarcinoma/metabolism-
dc.subject.MESHCarcinoma/pathology*-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHHumans-
dc.subject.MESHKangai-1 Protein/biosynthesis-
dc.subject.MESHKangai-1 Protein/genetics-
dc.subject.MESHKangai-1 Protein/physiology*-
dc.subject.MESHLung Neoplasms/enzymology*-
dc.subject.MESHLung Neoplasms/metabolism-
dc.subject.MESHLung Neoplasms/pathology*-
dc.subject.MESHMatrix Metalloproteinase 9/genetics-
dc.subject.MESHMatrix Metalloproteinase 9/metabolism*-
dc.subject.MESHMatrix Metalloproteinase Inhibitors*-
dc.subject.MESHNeoplasm Invasiveness/pathology-
dc.subject.MESHNeoplasm Invasiveness/prevention & control-
dc.subject.MESHRNA, Messenger/metabolism-
dc.subject.MESHTissue Inhibitor of Metalloproteinase-1/genetics-
dc.subject.MESHTissue Inhibitor of Metalloproteinase-1/physiology*-
dc.subject.MESHTransfection-
dc.subject.MESHUp-Regulation/physiology*-
dc.titleKAI1/CD82 suppresses tumor invasion by MMP9 inactivation via TIMP1 up-regulation in the H1299 human lung carcinoma cell line-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentMedical Research Center (임상의학연구센터)-
dc.contributor.googleauthorBo Keun Jee-
dc.contributor.googleauthorKoung Min Park-
dc.contributor.googleauthorSibin Surendran-
dc.contributor.googleauthorWoon Kyu Lee-
dc.contributor.googleauthorChang Whan Han-
dc.contributor.googleauthorYong Sik Kim-
dc.contributor.googleauthorYoung Lim-
dc.identifier.doi10.1016/j.bbrc.2006.01.153-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02996-
dc.relation.journalcodeJ00281-
dc.identifier.eissn1090-2104-
dc.identifier.pmid16488391-
dc.identifier.urlhttp://www.sciencedirect.com/science/article/pii/S0006291X06002439-
dc.subject.keywordH1299 non-small cell lung carcinoma cells-
dc.subject.keywordKAI1/CD82-
dc.subject.keywordMMP9-
dc.subject.keywordTIMP1-
dc.subject.keywordTumor invasiveness-
dc.contributor.alternativeNameLee, Woon Kyu-
dc.contributor.affiliatedAuthorLee, Woon Kyu-
dc.rights.accessRightsnot free-
dc.citation.volume342-
dc.citation.number2-
dc.citation.startPage655-
dc.citation.endPage661-
dc.identifier.bibliographicCitationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.342(2) : 655-661, 2006-
Appears in Collections:
1. College of Medicine (의과대학) > Medical Research Center (임상의학연구센터) > 1. Journal Papers

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