RESUMO
PURPOSE: Cyclooxygenase (COX)-2, an inducible enzyme that catalyzes the formation of prostaglandins from arachidonic acid, is overexpressed in various cancers, including prostate cancer, and cell lines. COX-2 has been reported to play an important role in carcinogenesis. The aim of this study was to evaluate the effects of a selective COX-2 inhibitor (meloxicam) on the cell proliferation, apoptosis, Bcl-2, and Bcl-xL expression in prostate cancer. MATERIALS AND METHODS: 20 male nude mice were subcutaneously inoculated with 1 million PC-3 cells expressing COX-2. After 1 week, the mice were divided into two groups of 10 mice. Group 1 was left untreated, which served as a control. Group 2 was treated with meloxicam (40mg/kg) four times a week for 3 weeks. After the 4 weeks experimental period, the tumors were immunohistochemically assayed for apoptosis (TUNEL) and proliferation (Ki-67). The COX-2, Bcl-2 and Bcl-xL mRNA expression levels in the tumors were evaluated by RT-PCR. RESULTS: The meloxicam had no effect on the tumor cell proliferation, but induced inhibition of PC-3 tumor cell growth and apoptosis. The Bcl-2 expression decreased in the meloxicam-treated group, but there was no significant difference between the two groups. The Bcl-xL expression was significantly down regulated in the meloxicam-treated group (p<0.01). CONCLUSIONS: Our results suggest that a selective COX-2 inhibitor suppresses PC-3 cell tumor growth in vivo. Tumor growth suppression was achieved by the induction of tumor cell apoptosis, and was associated with a decreased Bcl-xL expression, which is one of the Bcl-2 related genes.
