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Visit our Expo - Redox and Inflammation signaling 2012

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Session IX. Novel compounds targeting inflammatory <strong>signaling</strong> pathways Poster IX, 4<br />

The Cyclooxygenase-2 Selective Inhibitor Celecoxib Suppresses matrix<br />

Metalloproteinase <strong>and</strong> Inhibits in Vitro Invasion of the Human Oral Squamous<br />

Carcinoma cells<br />

Young E. Kwak, Nam K. Jeon, Jin Kim <strong>and</strong> Eun J. Lee<br />

Department of Oral Pathology, Oral Cancer Research Institute, BK21 project for<br />

Medical Science, Yonsei University College of Dentistry, Seoul, KOREA, 120-752<br />

E-mail: e16lee@yumc.yonsei.ac.kr<br />

Cyclooxygenease-2(COX-2) expression is a critical factor in inflammation, <strong>and</strong> plays an<br />

important role in defense against exogenous stimuli, while overexpression of COX-2 causes<br />

cells to exhibit changes in tumor phenotype. Recently, celecoxib was shown to reduce the risk<br />

of development of cancer <strong>and</strong> mortality from it. Tumor metastasis is the most important cause<br />

of cancer death. The present study attempted to determine the effects of celecoxib with regard<br />

to human oral squamous cell carcinoma(OSCC) cell growth <strong>and</strong> invasion/migration. The YD-<br />

10B cells represented a highly-invasive human oral squamous cell carcinoma(OSCC) cell line<br />

which was found to express the COX-2 protein. Celecoxib inhibited cell invasion/migration<br />

through the type 1 collagen matrix by ~ 60% within 24 h<strong>our</strong>s. Gelatin-based zymography<br />

assay reveal that, in the presence of 10uM celecoxib, both MMP-2 <strong>and</strong> MMP-9 enzyme<br />

activity decreased by ~25-30%. The current in vitro study indicated that the inhibition of<br />

invasion/migration in OSCC cell lines by the cyclooxgenase-2 specific inhibitor, celecoxib,<br />

results in anticancerous effects via a MMP-2 <strong>and</strong> MMP-9 suppression. In addition, YD-10B<br />

cells could be useful to study the pathological mechanism of OSCC. (This study was<br />

supported by the BK21 project for Medical Science, <strong>and</strong> by a grant of the national Cancer<br />

control R&D Program 2003(No. 0320230), Ministry of Health & Welfare, Republic of<br />

Korea.)<br />

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