• Jun Qin, Jianlin Yuan, Ling Li, Heliang Liu, Rongliang Qin, Weijun Qin, Baoqi Chen, He Wang, and Kaichun Wu.
• Department of Urology, Xijing Hospital, The Fourth Military Medical University, Xi'an 710032, PR China.
• Biomed. Pharmacother. 2009 Mar 1; 63 (3): 241-8.

AbstractOverexpression of cyclooxygenase (COX)-2 is associated with the progression of various malignancies, but the contribution of COX-2 expression, bioactivity or their cooperation to bladder cancer growth calls for further clarification. In this study, we investigated the inhibitory effect of COX-2 inhibitors, antisense COX-2 nucleotide, and their combination on the growth of bladder cancer cells (5637, 5637-P and 5637-AS). Suppression of either COX-2 expression or activity caused reduced cell proliferation, enhanced cell numbers in G(1) phase, and increased apoptosis; the joint suppression of COX-2 expression and bioactivity enhanced the degree of cell growth inhibition. COX-2 antisense-expressing 5637-AS tumors showed a 41.42+/-3.08% growth inhibition as compared with 5637 controls. Oral administration of indomethacin (3mg/kg) or celecoxib (15 mg/kg) caused tumor growth inhibition by 31.5+/-14.87% or 83.17+/-1.17%, respectively. When COX-2 antisense cDNA and COX-2 inhibitor celecoxib were combined, the tumor growth inhibition rate was further increased up to 88.78+/-3.10%. These results provide evidence that celecoxib has potential therapeutic effect on bladder cancer, and the joint use of COX-2 antisense cDNA with celecoxib may improve their individual therapeutic effect, especially significantly increase the growth inhibitory effect of COX-2 antisense cDNA.

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