• meloxicam;
  • COX-2 inhibitor;
  • ciglitazone;
  • PPARγ ligand;
  • ovarian cancer



It was recently reported that high expression of peroxisome proliferator-activated receptor γ (PPARγ) and low expression of cyclooxygenase-2 (COX-2) might be involved in the inhibition of ovarian tumor progression and confirmed that PPARγ activation could suppress COX-2 expression via the nuclear factor-κB pathway in ovarian cancer cells.


The current study investigated whether meloxicam, a selective COX-2 inhibitor, and ciglitazone, a ligand for PPARγ, inhibit the growth of human ovarian cancer cell lines and aimed to elucidate the molecular mechanism of their antitumor effect. Tumor growth and survival were examined in female nu/nu mice xenografted with subcutaneous OVCAR-3 tumors or with intraperitoneal DISS tumors and treated with meloxicam (162 ppm in diet, every day) or ciglitazone (15 mg/kg intraperitoneally once a week).


Both meloxicam and ciglitazone treatments significantly suppressed the growth of OVCAR-3 tumors xenotransplanted subcutaneously and significantly prolonged the survival of mice with malignant ascites derived from DISS cells as compared with controls. Meloxicam treatment decreased COX-2 expression in tumors by 2.5-fold compared with that observed in untreated tumors. Although ciglitazone treatment did not alter COX-2 expression in tumors, it reduced the expression of microsomal prostaglandin (PG) E synthase, which converts COX-derived PGH2 to PGE2. Both meloxicam and ciglitazone decreased PGE2 levels in serum as well as in ascites. Reduced microvessel density and induced apoptosis were found in solid OVCAR-3 tumors treated with either meloxicam or ciglitazone.


These results indicate that both meloxicam and ciglitazone produce antitumor effects against ovarian cancer in conjunction with reduced angiogenesis and induction of apoptosis. Cancer 2007; 110:791–800. © 2007 American Cancer Society.