Effect of gambogic acid on proliferation of SKM-1 cells and its mechanism.
10.7534/j.issn.1009-2137.2013.01.022
- Author:
Yun-Yu SUN
1
;
Shu-Jun WANG
;
Bao-An CHEN
;
Guo-Hua XIA
;
Jia-Hua DING
;
Chong GAO
;
Hui-Hui SONG
;
Qing-Long GUO
;
Hai-Wei ZHANG
;
Chun-Rui LI
;
Jian-Feng ZHOU
Author Information
1. Department of Hematology, Southeast University Medical School, Nanjing, Jiangsu Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Cycle Checkpoints;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Humans;
Myelodysplastic Syndromes;
metabolism;
pathology;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
Xanthones;
pharmacology;
bcl-2-Associated X Protein;
metabolism
- From:
Journal of Experimental Hematology
2013;21(1):105-109
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to explore the effect of gambogic acid (GA) on MDS SKM-1 cell proliferation, apoptosis and their possible mechanism. Cell proliferation was determined by MTT method. The apoptosis percentage and cell cycle regulation of SKM-1 cells were analyzed by flow cytometry. Morphological features were observed by light microscopy. The mRNA expression of bcl-2 and bax were detected by RT-PCR. The results showed that GA could inhibit the proliferation of SKM-1 cells in a dose- and time-dependent manner (IC50 was 0.37 µg/ml at 48 h), increase the apoptotic percentage of SKM-1 cells, and arrest cell cycle at the G0/G1. The expression of bax mRNA was up-regulated while that of bcl-2 mRNA was down-regulated in SKM-1 cells treated with GA for 48 h. It is concluded that GA can induce apoptosis, which may be related to its effect of arresting cells at phase of G0/G1 and down-regulating bcl-2/bax ratio.
