DC Field | Value | Language |
---|---|---|
dc.contributor.author | Park, Jong-Min | ko |
dc.contributor.author | Kim, Aeyung | ko |
dc.contributor.author | Oh, Jang-Hee | ko |
dc.contributor.author | Chung, An Sik | ko |
dc.date.accessioned | 2013-03-06T20:59:59Z | - |
dc.date.available | 2013-03-06T20:59:59Z | - |
dc.date.created | 2012-02-06 | - |
dc.date.created | 2012-02-06 | - |
dc.date.issued | 2007-04 | - |
dc.identifier.citation | CARCINOGENESIS, v.28, no.4, pp.837 - 847 | - |
dc.identifier.issn | 0143-3334 | - |
dc.identifier.uri | http://hdl.handle.net/10203/88442 | - |
dc.description.abstract | Selenium, an essential biological trace element, reduces the incidence of cancer. Our previous studies show that selenite inhibits tumor invasion by suppressing the expression of matrix metalloproteinases (MMP) -2 and -9.Methylseleninic acid (MSeA), an immediate precursor of methylselenol, inhibits tumor cell growth in vitro and mammary carcinogenesis in vivo. In this study, we demonstrate that MSeA suppresses pro-MMP-2 activation in a dose-dependent manner induced by 12-O-tetradecanoylphorbol-13-acetate (PMA), and further decreases the invasiveness of HT1080 tumor cells. Membrane type-1-MMP (MT1-MMP) is a crucial element in the process of pro-MMP-2 activation. Pro-MMP-2 binds MT1-MMP, using tissue inhibitor of metalloproteinase-2 (TIMP-2) as an adaptor, by forming a trimolecular complex on the cell surface. MSeA blocked MT1-MMP in a dose-dependent manner, but not TIMP-2 expression. MMP-9 and TIMP-1 levels were not affected by MSeA. Selenite induced a decrease in protein levels of both pro-MMPs -9 and -2, but not active forms of pro-MMP-2. MT1-MMP expression is regulated by NF-kappa B. Our data show that the effect of MSeA on MT1-MMP expression is mediated through suppression of NF-kappa B activity. Methylselenol generated by selenomethionine (SeMet) and methioninase (METase) inhibited pro-MMP-2 activation induced by PMA, confirming the effect of MSeA on pro-MMP-2 activity. Moreover, ROS production induced by PMA was partly decreased in the presence of MSeA. This suppression of ROS production may be related to diminished NF-kappa B activity. Thus, our results suggest that MSeA blocks tumor invasion in vitro via inhibiting pro-MMP-2 activation mediated by suppression of MT1-MMP expression, which is regulated by the NF-kappa B signal pathway. | - |
dc.language | English | - |
dc.publisher | OXFORD UNIV PRESS | - |
dc.subject | JUNCTIONAL INTERCELLULAR COMMUNICATION | - |
dc.subject | HUMAN DERMAL FIBROBLASTS | - |
dc.subject | PROTEIN-KINASE-C | - |
dc.subject | MATRIX METALLOPROTEINASES | - |
dc.subject | CANCER PREVENTION | - |
dc.subject | SELENIUM METABOLITE | - |
dc.subject | DIETARY SUPPLEMENTATION | - |
dc.subject | GLUTATHIONE-PEROXIDASE | - |
dc.subject | THIOREDOXIN REDUCTASE | - |
dc.subject | TISSUE INHIBITORS | - |
dc.title | Methylseleninic acid inhibits PMA-stimulated pro-MMP-2 activation mediated by MT1-MMP expression and further tumor invasion through suppression of NF-kappa B activation | - |
dc.type | Article | - |
dc.identifier.wosid | 000245351500010 | - |
dc.identifier.scopusid | 2-s2.0-34047238470 | - |
dc.type.rims | ART | - |
dc.citation.volume | 28 | - |
dc.citation.issue | 4 | - |
dc.citation.beginningpage | 837 | - |
dc.citation.endingpage | 847 | - |
dc.citation.publicationname | CARCINOGENESIS | - |
dc.identifier.doi | 10.1093/carcin/bgl203 | - |
dc.contributor.nonIdAuthor | Park, Jong-Min | - |
dc.contributor.nonIdAuthor | Kim, Aeyung | - |
dc.contributor.nonIdAuthor | Oh, Jang-Hee | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordPlus | JUNCTIONAL INTERCELLULAR COMMUNICATION | - |
dc.subject.keywordPlus | HUMAN DERMAL FIBROBLASTS | - |
dc.subject.keywordPlus | PROTEIN-KINASE-C | - |
dc.subject.keywordPlus | MATRIX METALLOPROTEINASES | - |
dc.subject.keywordPlus | CANCER PREVENTION | - |
dc.subject.keywordPlus | SELENIUM METABOLITE | - |
dc.subject.keywordPlus | DIETARY SUPPLEMENTATION | - |
dc.subject.keywordPlus | GLUTATHIONE-PEROXIDASE | - |
dc.subject.keywordPlus | THIOREDOXIN REDUCTASE | - |
dc.subject.keywordPlus | TISSUE INHIBITORS | - |
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