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Objective: We studied the inhibitory effect of human cholangiocarcinoma line (QBC939) treated by selective cyclooxygenase-2 (COX-2) inhibitor NS-398 and provided the theoretical foundation for the clinical practice. Methods: Selec- tive COX-2 inhibitor NS-398 on the growth suppression was evaluated by MTT method. The apoptotic rate was quantified and cell cycle by flow cytometry (FCM). Invasive ability was detected by Transwell. The expression of vascular endothelial growth factor (VEGF) and COX-2 in cholangiocarcinoma line was determined by enzyme-linked immunosorbent assay (ELISA). Results: NS-398 could be time-dose dependently inhibited the growth, induced apoptosis, invasived ability, S phase was inhibited, down-regulate the expression of VEGF and COX-2 in cholangiocarcinoma line (QBC939). Conclusion: NS398 can inhibit proliferation of cholangiocarcinoma cell Iine QBC939 and inhibit the invasive ability and induce its apoptosis in vitro, which may contributed to the COX-2 dependent pathway to reduce the release of VEGF.
Objective: We studied the inhibitory effect of human cholangiocarcinoma line (QBC939) treated by selective cyclooxygenase-2 (COX-2) inhibitor NS-398 and provided the theoretical foundation for the clinical practice. Methods: Selectiv COX-2 inhibitor NS- 398 on the growth suppression was evaluated by MTT method. The apoptotic rate was quantified and cell cycle by flow cytometry (FCM). Invasive ability was detected by Transwell. The expression of vascular endothelial growth factor (VEGF) and COX-2 in cholangiocarcinoma line was determined by enzyme-linked immunosorbent assay (ELISA). Results: NS-398 could be time-dose dependently inhibited the growth, induced apoptosis, invasived ability, S phase was inhibited, down-regulate the expression of VEGF and COX- 2 in cholangiocarcinoma line (QBC939). Conclusion: NS398 can inhibit proliferation of cholangiocarcinoma cell Iine QBC939 and inhibit the invasive ability and induce its apoptosis in vitro, which may contribute to the COX-2 dependent pathway to reduce the release of VEGF.