Purpose: Tumor invasion and metastasis are known to be extremely
important factors in the prognosis of cancer patients. Although recent
studies have demonstrated that cyclooxygenase-2 (COX-2) is overexpressed in
various cancers including gastric cancer, the mechanisms underlying the
contribution of COX-2 to tumorigenesis and tumor promotion remain unclear.
Methods: In order to determine the role of COX-2 in tumor growth and
metastasis, we investigated COX-2 expression, apoptosis and the expression
of E-cadherin, CD44v6, MMP-2 and TIMP-2 in gastric cancer xenografts treated
with meloxicam (a selective COX-2 inhibitor). Results: Cells from the
MKN45 gastric cancer cell line that overexpress COX-2 were inoculated
subcutaneously into athymic mice. Oral administration with meloxicam reduced
the tumor volume (P<0.01), induced apoptosis of cancer cells (P<0.01),
suppressed the proliferation rates (P<0.01), increased the expression of
E-cadhrin (P<0.05) and reduced the expression of MMP-2 and TIMP-2.
Conclusion: The above data showed that COX-2 inhibitors can inhibit
tumor growth and suppress metastatic potential by expression of adhesion
molecules and suppression of metalloproteinases, suggesting that this
inhibitor can be used as an additive anti-cancer drug in cases of stomach
cancer with radical resection, although further evaluation is required.
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