Pro-MMP-2 activation by the PPARγ agonist, ciglitazone, induces cell invasion through the generation of ROS and the activation of ERK

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dc.contributor.authorK H Kim-
dc.contributor.authorYeesook Cho-
dc.contributor.authorJ M Park-
dc.contributor.authorS O Yoon-
dc.contributor.authorK W Kim-
dc.contributor.authorA S Chung-
dc.date.accessioned2017-04-19T09:07:41Z-
dc.date.available2017-04-19T09:07:41Z-
dc.date.issued2007-
dc.identifier.issn0014-5793-
dc.identifier.uri10.1016/j.febslet.2007.06.012ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/7981-
dc.description.abstractPeroxisome proliferator-activated receptor γ (PPARγ) is a nuclear receptor modulating a variety of biological functions including cancer cell proliferation and differentiation. However, the role of PPARγ and its ligands in tumor invasion is unclear. To evaluate a possible role for PPARγ ligands in tumor invasion, we examined whether PPARγ agonists including pioglitazone, troglitazone, rosiglitazone, and ciglitazone could affect the activity of matrix metalloproteinases (MMPs) in the HT1080 cell line, a well-studied and well-characterized cell line for MMP research. The gelatin zymography assay showed that ciglitazone activated pro-MMP-2 significantly. In addition, ciglitazone increased the expression of MMP-2, which was accompanied by an increase of membrane type 1-MMP (MT1-MMP) expression. The PPARγ antagonist, GW9662 attenuated the ciglitazone-induced PPARγ activation but it did not affect the pro-MMP2 activation by ciglitazone, suggesting that the action of ciglitazone on the pro-MMP-2 activation bypassed the PPARγ pathway. Antioxidants and various inhibitors of signal transduction were used to investigate the mechanism of ciglitazone-induced pro-MMP-2 activation. We found that the sustained production of reactive oxygen species (ROS) was required for pro-MMP-2 activation by ciglitazone. We also found that PB98059, an inhibitor of MEK-ERK, significantly blocked ciglitazone-induced pro-MMP-2 activation and that extracellular signal-regulated kinase (ERK) was hyperphosphorylated by ciglitazone. Moreover, cell invasion was significantly increased by ciglitazone in the HT1080 cell lines, whereas cell motility was not affected. This study suggests that ciglitazone-induced pro-MMP-2 activation increases PPARγ-independent tumor cell invasion through ROS production and ERK activation in some types of cancer cells.-
dc.publisherWiley-
dc.titlePro-MMP-2 activation by the PPARγ agonist, ciglitazone, induces cell invasion through the generation of ROS and the activation of ERK-
dc.title.alternativePro-MMP-2 activation by the PPARγ agonist, ciglitazone, induces cell invasion through the generation of ROS and the activation of ERK-
dc.typeArticle-
dc.citation.titleFEBS Letters-
dc.citation.number17-
dc.citation.endPage3310-
dc.citation.startPage3303-
dc.citation.volume581-
dc.contributor.affiliatedAuthorYeesook Cho-
dc.contributor.alternativeName김규한-
dc.contributor.alternativeName조이숙-
dc.contributor.alternativeName박종민-
dc.contributor.alternativeName윤상오-
dc.contributor.alternativeName김규원-
dc.contributor.alternativeName정안식-
dc.identifier.bibliographicCitationFEBS Letters, vol. 581, no. 17, pp. 3303-3310-
dc.identifier.doi10.1016/j.febslet.2007.06.012-
dc.subject.keywordciglitazone-
dc.subject.keywordextracellular signal-regulated kinase-
dc.subject.keywordmatrix metalloproteinase-2 activation-
dc.subject.keywordperoxisome proliferator-activated receptor γ agonists-
dc.subject.keywordreactive oxygen species production-
dc.subject.keywordtumor invasion-
dc.subject.localciglitazone-
dc.subject.localextracellular signal-regulated kinase-
dc.subject.localExtracellular Signal-Regulated Kinase-
dc.subject.localExtracellular signal regulated kinase (ERK)-
dc.subject.localExtracellular signal-regulated kinase-
dc.subject.localmatrix metalloproteinase-2 activation-
dc.subject.localperoxisome proliferator-activated receptor γ agonists-
dc.subject.localreactive oxygen species production-
dc.subject.localtumor invasion-
dc.description.journalClassY-
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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