Effects of sinensetin on proliferation and apoptosis of human gastric cancer AGS cells.
- Author:
Yang DONG
1
;
Guang JI
;
Aili CAO
;
Jianrong SHI
;
Hailian SHI
;
Jianqun XIE
;
Dazheng WU
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Cell Line, Tumor; Cell Proliferation; drug effects; Cyclin-Dependent Kinase Inhibitor p21; analysis; Dose-Response Relationship, Drug; Flavonoids; pharmacology; Humans; Stomach Neoplasms; drug therapy; pathology; Tumor Suppressor Protein p53; analysis
- From: China Journal of Chinese Materia Medica 2011;36(6):790-794
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effects and mechanisms of sinensetin on proliferation and apoptosis of human AGS gastric cancer cells.
METHODMTT assay was used to detect the growth inhibition rates of human AGS gastric cancer cells treated with sinsesectin in different concentrations and times. The cell cycle distribution was measured by flow cytometry. The apoptosis was examined by Annexin-FITC/PI staining and DNA fragment analysis. The apoptosis morphology was observed by inverted fluorescence microscope after Hoechst 33342 staining. The protein expressions of p21 and p53 were detected by western blot.
RESULTMTT assay showed that sinensetin inhibited the growth of AGS gastric cancer cells in a dose- and time-dependent manner. Sinensetin blocked AGS cells in G2/ M and increased the apoptosis rates of AGS cells in a dose-dependent manner. DNA ladder was observed in cells treated with 60 micromol x L(-1) sinensetin for 48 h. The typical apoptotic morphological changes including cell nucleus shrinkage, chromatin condensation and apoptotic bodies were observed when treated with different dose of sinensetin. Western blot showed that sinensetin increased expressions of p53 and p21 in a dose-dependent manner.
CONCLUSIONSinensetin could inhibit human AGS gastric cancer cells proliferation and induce cell cycle block in G2/M phase and apoptosis. The up regulation of p53 and p21 protein might be one of the mechanisms.