Mechanism of apoptosis induced by specific COX-2 inhibitor SC236 in gastric cancer cells.
- Author:
Xiao-ming FAN
1
;
Fa-shou ZHENG
;
Hong-yan LIU
;
Yuan-hua MA
;
B C Y WONG
Author Information
- Publication Type:Journal Article
- MeSH: Adenocarcinoma; metabolism; pathology; Apoptosis; drug effects; Caspase 3; Caspases; metabolism; Cell Line, Tumor; Cyclooxygenase 2 Inhibitors; pharmacology; Cytochromes c; metabolism; Humans; Oligopeptides; pharmacology; Poly(ADP-ribose) Polymerases; metabolism; Pyrazoles; pharmacology; Stomach Neoplasms; metabolism; pathology; Sulfonamides; pharmacology; bcl-2 Homologous Antagonist-Killer Protein; metabolism
- From: Chinese Journal of Oncology 2005;27(3):145-147
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the underlying mechanism of apoptosis-inducing effect of a specific COX-2 inhibitor SC236 in gastric cancer cells.
METHODSWestern blot analysis was used to measure apoptosis-related proteins, cytochrome c, and caspase-3. The catalytic activity of the caspases was measured using a colorimetric assay.
RESULTSTreatment of AGS gastric cancer cells with SC236 caused a significant elevation of the pro-apoptotic protein Bak, release of cytochrome c to the cytosol, and activation of caspase-3. A specific caspase-3 inhibitor, z-DEVD-fmk, blocked SC236-induced apoptosis.
CONCLUSIONSC236 inhibits cell growth and induces apoptosis in gastric cancer cells at least partly through the up-regulation of Bak, stimulation of cytochrome c release, and activation of caspase-3.