S-Space College of Medicine/School of Medicine (의과대학/대학원) Internal Medicine (내과학전공) Journal Papers (저널논문_내과학전공)
The anti-cancer effect of COX-2 inhibitors on gastric cancer cells
- Cho, Soo-Jeong; Kim, Nayoung; Kim, Joo Sung; Jung, Hyun Chae; Song, In Sung
- Issue Date
- Springer Verlag
- Dig Dis Sci. 2007 Jul;52(7):1713-21. Epub 2007 Mar 28.
- Adenocarcinoma/*drug therapy/metabolism; Apoptosis/drug effects; Cell Cycle/drug effects; Cell Line, Tumor; Cyclooxygenase 2 Inhibitors/pharmacology/*therapeutic use; Dinoprostone/metabolism; Humans; Microscopy, Fluorescence; Pyrazoles/pharmacology/*therapeutic use; Stomach Neoplasms/*drug therapy/metabolism; Sulfonamides/pharmacology/*therapeutic use; Tetrazolium Salts/diagnostic use; Thiazoles/diagnostic use
- Epidemiologic studies have shown that nonsteroidal anti-inflammatory drugs could reduce the risk of cancer development including gastric cancer. This study was performed to identify the antineoplastic mechanism in gastric cancer cells affected by celecoxib, a selective COX-2 inhibitor. MTT assay, ELISA for prostaglandin E(2) (PGE(2)), cell-cycle analyses, immunofluorescent staining, and flow cytometry were performed after treating human gastric cancer cell lines (AGS and MKN-45) with celecoxib or indomethacin. The viabilities of celecoxib-treated cells decreased in a dose- and time-dependent manner compared with indomethacin. Drop of PGE(2) levels was more prominent in the presence of indomethacin than in that of celecoxib. Celecoxib arrested the cell cycle in the G(0)-G(1) phase, which reduced cell numbers in the S phase. Moreover, celecoxib increased the apoptotic cell proportions, a 4-fold increase over control cells. The anticancer effects of celecoxib on gastric cancer cells appear to be mediated by cell-cycle arrest and apoptosis, and not by COX-2 or PGE(2) suppression alone.
- 0163-2116 (Print)
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