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Journal of Cancer Prevention

Original

Cancer prevention research 2006; 11(2): 89-98

Published online June 30, 2006

© Korean Society of Cancer Prevention

The Mechanism of Cell Growth Inhibition and Apoptosis by Cyclooxygenase-2 Inhibitior in Oral Squamous Carcinoma Cells

Young Eun Kwak, Nam Kyeong Jeon, Jin Kim and Eun Ju Lee

Abstract

Recently, prostaglandins have been reported to influence cell proliferation resulting in cancer development and progression. Prostaglandins are synthesized by cyclooxygenase (COX) pathway, COX-1 is constituently present in most cells and tissues where produce prostaglandins, while COX-2 expression is a critical part of inflammation and plays a major role in defending against exogenous stimuli. Moreover, COX-2 has been known to be related to cancer progression. Accordingly, cancer prevention trials have been applied by use of COX-2 inhibitors. Several putative targets have been proposed to account for NSAID-induced growth inhibition and apoptosis. This study was aimed at investigating the growth inhibitory effect and apoptosis mechanism by selective COX-2 inhibitor, celecoxib, in human oral squamous carcinoma cancer (OCC) cell lines. As a results, Celecoxib inhibited the growth of the cell lines in a dose dependent manner. Cell cycle kinetic analysis demonstrated that Celcoxib induces a delay in cll cycle progression and a G1 arrest. This induction of a G1 arrest was associated with the up-regulation of cyclin dependent kinase inhibitors (CDKI) p27KIP1 and P21CIP/WAF1. In adddition, 70 uM Celecoxib induced apoptosis through caspase-3 pathway. In conclusion, this study indicates that COX-2 specific inhibitor celecoxib induces apoptosis and cell cycle arrest in two oral squamous carcinoma cell lines. (Cancer Prev Res 11, 89-98, 2006)

Keywords: Oral squamous carcinoma cell lines, Celecoxib, Cell cycle, Apoptosis, Cyclooxygenase

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