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J.P. Souza Filho, Z.M. Correa, J.–C.A. Marshall, A.B. Coutinho, M.C. Martins, M.N. Burnier, Jr; The Effect of a Selective Cyclooxygenase–2 (COX–2) Inhibitor on the Proliferative Rate of Retinoblastoma Cell Lines . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3418.
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Purpose: The expression of COX–2 has previously been demonstrated in retinoblastoma. A previous study has suggested that a relationship exists between the expression of COX–2 and the genesis of retinoblastoma. COX–2 expression induces a variety of cytokines that can alter cellular proliferation, invasion, and apoptotic processes. The aim of this study is to examine the effect of nepafenac, a selective COX–2 inhibitor, on the proliferative rate of two human retinoblastoma cell lines. Methods: Two human retinoblastoma cell lines, WERI and Y79, were used. The cells were grown in RPMI 1640 geneticin selective medium supplemented with 10% Fetal Bovine Serum. COX–2 expression in the cell lines was verified by imunocytochemical analysis of cytospin sections. An MTT based proliferation assay was used to compare retinoblastoma cell growth with and without amfenac, the active metabolite of nepafenac. All cell lines were seeded at a concentration of five thousand cells per well in a ninety–six well plate. Amfenac, at the recommended IC50 of 150 nM, was added to the experimental wells of each cell line, while RPMI was added to the control wells. Cells were incubated for 48 hours and then mitochondrial activity was assayed using the MTT assay. The averaged results per condition were recorded. The Student’s t – test was used to compare results from the cells cultured with and without amfenac. Results: The Y79 cell line showed a higher proliferative rate than the WERY–1 cell line. Immunocytochemical analysis revealed that both cell lines were COX–2 negative in vitro. However, the addition of amfenac to both of the cell lines gave a statistically significant reduction (P < 0.005) in proliferation in both cell lines. Conclusions: The selective anti–COX–2 molecule amfenac inhibited proliferation of both tested retinoblastoma cell lines despite the fact that both cell lines were negative for COX–2 expression. This may indicate that a secondary pathway is involved in the effect of amfenac upon cellular proliferation. Further trials should be undertaken to study the effect of selective COX–2 inhibitors on retinoblastoma.
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