Effects of simvastatin on proliferation and apoptosis of acute monocytic leukemia cell line SHI-1.
- Author:
Yan-Fen LI
1
;
Ri ZHANG
;
Xu-Hui ZHANG
;
Guang-Hua CHEN
;
Jian-Nong CEN
;
Zi-Ling ZHU
Author Information
1. Key Laboratory of Thrombosis and Hemostasis Subordinated to Ministry of Health, Jiangsu lnsititute of Hematology, Suzhou University First Affiliated Hospital, Suzhou 215006, Jiangsu Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Caspase 3;
metabolism;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Gene Expression Regulation, Leukemic;
Humans;
Leukemia, Monocytic, Acute;
pathology;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
Simvastatin;
pharmacology
- From:
Journal of Experimental Hematology
2011;19(3):612-616
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of this study was to investigate the effect of simvastatin (SIM) on proliferation and apoptosis of acute monocytic leukemia cell line SHI-1 and its mechanism. Experiments were divided into control and test groups (5 µmol/L, 10 µmol/L, 20 µmol/L SIM groups). The growth inhibitory rate of SHI-1 cells was detected using methyl thiazolyl tetrazolium (MTT) method. The cell cycle distribution and apoptotic rate were measured by using flow cytometry. The expression of BCL-2, caspase-3 mRNA were determined by reverse transcription polymerase chain reaction (RT-PCR). The expression of BCL-2, caspase-3 protein levels were analyzed by Western blot. The results demonstrated that SIM inhibited the growth of SHI-1 cells in time- and does-dependent manners. Cell cycle analysis showed that SHI-1 cells significantly arrested in S phase (p < 0.05) after treating with SIM for 48 hours, as compared with control group. 5 µmol/L SIM in test group significantly blocked cell cycle progression, but can not induce apoptosis. The expressions of BCL-2 mRNA and protein were down-regulated and caspase-3 mRNA and protein were up-regulated along with the increase of SIM concentration (p < 0.05). It is concluded that SIM is able to inhibit proliferation and induce apoptosis of SHI-1 cells, the mechanism may be associated with downregulating the expression of apoptosis-related gene BCL-2, upregulating the expression of caspase-3.
