N-Acetylglucosaminyltransferase V triggers overexpression of MT1-MMP and reinforces the invasive/metastatic potential of cancer cells

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dc.contributor.authorJu Hee Lee-
dc.contributor.authorJeong Gu Kang-
dc.contributor.authorKyoung Jin Song-
dc.contributor.authorSeong Kook Jeon-
dc.contributor.authorS Oh-
dc.contributor.authorYong Sam Kim-
dc.contributor.authorJeong Heon Ko-
dc.date.accessioned2017-04-19T09:38:54Z-
dc.date.available2017-04-19T09:38:54Z-
dc.date.issued2013-
dc.identifier.issn0006-291X-
dc.identifier.uri10.1016/j.bbrc.2013.01.065ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/11279-
dc.description.abstractN-Acetylglucosaminyltransferase V (GnT-V) is an enzyme that catalyzes the formation of a β1,6. N-acetylglucosamine (GlcNAc) side chain to a core mannosyl residue in N-linked glycoproteins. Besides its direct function of producing aberrant glycoproteins, it promotes cancer progression by its involvement in the stimulation of oncoproteins. Herein, we report that GnT-V guided the transcriptional activation of membrane-type matrix metalloproteinase-1 (MT1-MMP) in cancer cells. The activated MT1-MMP expression had dual effects on cancer progression. It not only promoted proteolytic activity for cancer cells per se, but also led to the activation of MMP-2. Consequently, the activation of the two MMPs triggered by GnT-V intensified the invasive potential. A quantitative analysis using clinical tissues revealed a relatively strong correlation between GnT-V overexpression and MT1-MMP upregulation. In this study, we report for the first time that GnT-V directs cancer progression by modulating MMPs in cancer.-
dc.publisherElsevier-
dc.titleN-Acetylglucosaminyltransferase V triggers overexpression of MT1-MMP and reinforces the invasive/metastatic potential of cancer cells-
dc.title.alternativeN-Acetylglucosaminyltransferase V triggers overexpression of MT1-MMP and reinforces the invasive/metastatic potential of cancer cells-
dc.typeArticle-
dc.citation.titleBiochemical and Biophysical Research Communications-
dc.citation.number4-
dc.citation.endPage663-
dc.citation.startPage658-
dc.citation.volume431-
dc.contributor.affiliatedAuthorJu Hee Lee-
dc.contributor.affiliatedAuthorJeong Gu Kang-
dc.contributor.affiliatedAuthorKyoung Jin Song-
dc.contributor.affiliatedAuthorSeong Kook Jeon-
dc.contributor.affiliatedAuthorYong Sam Kim-
dc.contributor.affiliatedAuthorJeong Heon Ko-
dc.contributor.alternativeName이주희-
dc.contributor.alternativeName강정구-
dc.contributor.alternativeName송경진-
dc.contributor.alternativeName전성국-
dc.contributor.alternativeName오세정-
dc.contributor.alternativeName김용삼-
dc.contributor.alternativeName고정헌-
dc.identifier.bibliographicCitationBiochemical and Biophysical Research Communications, vol. 431, no. 4, pp. 658-663-
dc.identifier.doi10.1016/j.bbrc.2013.01.065-
dc.subject.keywordGnT-V-
dc.subject.keywordMMP-2-
dc.subject.keywordMT1-MMP-
dc.subject.keywordTumor progression-
dc.subject.localGnT-V-
dc.subject.localMMP-2-
dc.subject.localMMP2-
dc.subject.localMT1-MMP-
dc.subject.localtumor progression-
dc.subject.localTumor progression-
dc.subject.localTumor Progression-
dc.description.journalClassY-
Appears in Collections:
Synthetic Biology and Bioengineering Research Institute > Genome Editing Research Center > 1. Journal Articles
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