NS398 induced apoptosis in pancreatic carcinoma cell strain BxPC-3 through a COX-2-in dependent pathway.
- Author:
Dong-sheng HUANG
1
;
Xiao XU
;
Shu-sen ZHENG
;
Jian-feng CHENG
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Caspase 3; drug effects; metabolism; Cyclooxygenase 1; metabolism; Cyclooxygenase 2; metabolism; Cyclooxygenase Inhibitors; pharmacology; Humans; Nitrobenzenes; pharmacology; Pancreatic Neoplasms; enzymology; pathology; Sulfonamides; pharmacology; Tumor Cells, Cultured
- From: Acta Academiae Medicinae Sinicae 2005;27(5):601-605
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of the selective cyclooxygenase-2 (COX-2) inhibitor NS398 on the growth of human pancreatic tumor BxPC-3 cell strain and its possible mechanisms.
METHODSThe effect of NS398 on cell growth was assessed by 3- (4,5-dimethylthiazol-2-yl) -2, 5-diphenyl thiazolyl blue (MTT) assay. Apoptosis was determined by fluorescence-activated cell scanning (FACS) analysis and assessment of the floating cell/attached cell ratio. Caspase-3 activation was evaluated by Active Caspase-3 Apoptosis Kit with flow cytometry. Reverse transcriptase-polymerase chain reaction analysis (RT-PCR) and Western blot were used to demonstrate expression levels of COX-1, COX-2 mRNA, and protein, as well as Caspase-3 protein in pancreatic tumor BxPC-3 cell strain.
RESULTSSelective COX-2 inhibitor NS398 significantly decreased cell viability and induced apoptosis in pancreatic tumor BxPC-3 cell strain. The protein expression of Caspase-3 was induced by high-concentration NS398. Caspase-3 activity was strongly activated by NS398.
CONCLUSIONSSelective COX-2 inhibitor NS398 has antiproliferative and proapoptotic potential in pancreatic tumor BxPC-3 cells. Such effect is independent of COX-2, but correlates with Caspase-3 activation.
