Inhibition of gastric cancer cells growth in vitro by sulindac.
- Author:
Dong-Hong YU
1
;
Lei ZHOU
;
Ping WANG
;
Qi-Zhi WANG
;
Ze-Nong CHENG
Author Information
- Publication Type:Journal Article
- MeSH: Antineoplastic Agents; administration & dosage; pharmacology; Apoptosis; drug effects; Cell Cycle; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Cyclooxygenase 2; metabolism; Dose-Response Relationship, Drug; Humans; Ki-67 Antigen; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism; Stomach Neoplasms; metabolism; pathology; Sulindac; administration & dosage; pharmacology
- From: Chinese Journal of Oncology 2006;28(7):498-502
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of sulindac on proliferation and apoptosis of human gastric cancer BGC-823 cells and its antineoplastic mechanisms.
METHODSHuman gastric cancer BGC-823 cells were incubated with sulindac at various concentrations and for different times. Morphological changes of BGC-823 cells were observed under an inversion microscope. MTT colorimetric assay was used to examine the effect of sulindac on the proliferation of BGC-823 cells. Flow cytometry was used to determine the cell cycle distribution and apoptosis. Transmission electron microscopy was performed to examine cell apoptosis morphology. Immunohistochemical staining was used to detect the expressions of COX-2, bcl-2 and ki-67 in the cells.
RESULTSsulindac induced morphologic alterations in BGC-823 cells, inhibited cell proliferation, increased the proportion of cells in G0/G1 phase and decreased the proportion of cells in S phase, induced apoptosis of BGC-823 cells, and decreased expressions of COX-2, bcl-2, ki-67 in the cells. All the effects were in a time- and dose-dependent manner (P < 0.05). Some characteristic morphologic features of apoptosis were revealed by transmission electron microscopy.
CONCLUSIONsulindac may inhibit the growth of gastric cancer BGC-823 cells in vitro and the anti-tumor mechanism may be related to changes in cell cycle distribution, induction of apoptosis and inhibition of expression of COX-2, bcl-2, and ki-67.