Cyclooxygenase-2 (COX-2) participates in
cancer invasion and
metastasis by decreasing the expression of
E-cadherin. However, the molecular mechanisms through which COX-2 regulates
E-cadherin expression and function have not yet been fully elucidated. The aim of this study was to investigate the possible molecular mechanisms through which COX-2 regulates
E-cadherin expression in
gastric cancer. The
mRNA and
protein expression of COX-2, nuclear factor-κB (NF-κB), Snail and
E-cadherin was detected in
gastric cancer cells by quantitative PCR and western blot analysis, respectively. The expression of these genes was also detected in healthy gastric mucosa and
gastric cancer tissues by immunohistochemistry. We detected various levels of COX-2, nuclear factor-κB (NF-κB), Snail and
E-cadherin expression in the normal gastric mucosa and
cancer tissues; however, the expression patterns differed: the increased expression of COX-2, NF-κB and Snail was observed in the
gastric cancer tissues, whereas there was a considerable reduction in
E-cadherin expression in the
cancer tissues compared to the normal gastric mucosa. The expression patterns of COX-2, NF-κB and Snail were similar. The increased expression of COX-2 in the
gastric cancer tissues closely correlated with the increased expression of NF-κB and Snail, but inversely correlated with the expression of
E-cadherin. Treatment of the SGC7901 cells (which express high levels of COX-2) with
celecoxib, a
COX-2 inhibitor, not only led to a marked dose- and time-dependent decrease in the expression of COX-2, NF-κB and Snail, but also led to a significant increase in the expression of
E-cadherin, and this was associated with a reduction in cell invasion. By contrast, the same treatment did not alter the expression of these genes in another
gastric cancer cell line, MGC803 (which barely expresses COX-2). These data suggest that COX-2 regulates the expression of
E-cadherin through the NF-κB and Snail signaling pathway in
gastric cancer.