Celecoxib Inhibits Proliferation and Induces Apoptosis via Cyclooxygenase-2 Pathway in Human Pancreatic Carcinoma Cells

• Published in: Current medical science 2005, Vol.25 (1), p.42-44
• Main Author: 吴高松 易继林 邸方 邹声泉 李兴睿
• Format: Article
• Language: English
• Subjects: Apoptosis - drug effects; Celecoxib; Cell Proliferation - drug effects; Cyclooxygenase 2 - metabolism; Cyclooxygenase Inhibitors - pharmacology; Dinoprostone - metabolism; Humans; Pancreatic Neoplasms - pathology; Pyrazoles - pharmacology; Sulfonamides - pharmacology; Tumor Cells, Cultured; 环氧合酶-2; 细胞增殖; 肿瘤细胞; 胰腺癌
• ISSN: 1672-0733; 2096-5230; 1993-1352; 2523-899X
• DOI: 10.1007/bf02831383

In order to evaluate the effects and mechanisms of celecoxib in inhibiting proliferation and inducing apoptosis on human pancreatic carcinoma cells, the anti-proliferative effect was measured by using methabenzthiazuron (MTT) assay. Cell cycle and apoptosis were analyzed by using flow cytometry (FCM), and the PGE2 levels in the supernatant of cultured pancreatic carcinoma cells were quantitated by enzyme-linked immunoabsordent assay (ELISA). Our results showed that celecoxib suppressed the production of PGE2 and inhibited the growth of JF-305 cells, and the anti-proliferative effect of celecoxib could be abolished by addition of PGE2. FCM revealed that celecoxib could inhibit proliferation and induce apoptosis by G1 S cell cycle arrest. It was concluded that cyclooxygenase-2 specific inhibitor celecoxib could inhibit proliferation and induced apoptosis of human pancreatic carcinoma cells via suppression of PGE2 production in vitro.