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Pancreatic cancer is the fourth leading cause of cancer-associated cases of mortality worldwide. Prostaglandin-endoperoxide synthase 2 (COX-2) is considered a therapeutic target for prevention of pancreatic cancer. Nimesulide, a selective COX-2 inhibitor, can induce cell apoptosis, resulting in an anti-cancer effect. However, the mechanism underlying this effect remains to be elucidated. The present study aimed to evaluate the effects of nimesulide on proliferation of PANC-1 cells using an MTT assay. Apoptosis was evaluated by DNA laddering and Annexin V-fluorescein isothiocyanate/propidium iodide-stained flow cytometry. Furthermore, western blot analysis was used to elucidate the mechanism underlying nimesulide treatment in PANC-1 cells. It was determined that proliferation of PANC-1 cells was inhibited by nimesulide in a dose-dependent manner. Nimesulide promoted apoptosis of PANC-1 cells. Western blot analysis demonstrated that nimesulide increased expression of cleaved caspase-3 and apoptosis regulator Bax (Bcl-2 associated protein X), and decreased the expression of pro-caspase-3 and apoptosis regulator Bcl-2 (B-cell lymphoma 2). Furthermore, nimesulide enhanced expression of phosphatase and tensin homolog (PTEN), and decreased the expression level of COX-2 and vascular endothelial growth factor. In summary, the results of the present study demonstrated that nimesulide could induce apoptosis and inhibit growth of PANC-1 cells by enhancing the expression of PTEN, which indicates the potential of nimesulide to prevent tumor angiogenesis.

Nimesulide inhibits proliferation and induces apoptosis of pancreatic cancer cells by enhancing expression of PTEN