Abstract: The Effects of NS398, a Selective Cyclooxygenase-2 Inhibitor, on Proliferation and Apoptosis ofHuman Breast Cancer Cell Line MCF-7 and Its MolecularMechanismTingting LIU, Zhongsheng TONG, Yehui SHI, Chunfang HAOCorrespondence to: Zhongsheng TONG, E-mail: tonghang@medmail.com.cnDepartment of Medicinal Oncology of Breast, Tianjin Medical University Cancer Institute and Hospital, Tianjin 300060, ChinaKey Laboratory of Breast Cancer Prevention and Therapy, Tianjin Medical University, Ministry of Education. Key Laboratory of Can-cer Prevention and Therapy, Tianjin 300060, ChinaThis work was supported by a grant from Natural Science Foundation of Tianjin (No. 10JCYBJC11500)Abstract Objective: To investigate the anti-neoplastic effects of selective cyclooxygenase-2 inhibitor NS398 on proliferationand apoptosis of human breast cancer cell line MCF-7, and to preliminarily explore its molecular mechanism. Methods: MCF-7 cellswere treated with NS398 at different concentrations for a period ranging from 24 to 72 hours. MTT assay was used to detect the prolifer-ation of MCF-7 cells. Flow cytometry ( Annexin V-FITC/PI ) was performed to analyze the apoptosis of MCF-7 cells. The expressionof COX-2 was measured by Western blot, and the levels of VEGF and PGE2 were measured by ELISA. Results: NS398 inhibited prolif-eration of the MCF-7 cells. The inhibitory effect varied with the different concentrations of NS398 and the exposure time. Across a sin-gle drug exposure time period, there were statistical differences among the 4 concentrations of NS398, i.e., 10 μmol/L, 20 μmol/L, 40μmol/L and 80 μmol/L ( P < 0.001 ). NS398 downregulated the expression of COX-2 protein in MCF-7 cells. Levels of VEGF andPGE2 were suppressed by NS398. There was a significant negative correlation between the apoptotic rate of MCF-7 cells and the levelsof VEGF and PGE2. Conclusion: NS398 inhibits the proliferation of human breast cancer cell line MCF-7 and induces apoptosis. Themechanism may be associated with downregulation of COX-2 and inhibition of VEGF and PGE2.Keywords Breast cancer; Cyclooxygenase-2; NS398; Growth inhibition