Effect of rapamycin on apoptosis in human myelodysplastic syndrome cell line MUTZ-1 and its possible mechanisms.
- Author:
Bao-Guo CHEN
1
;
Qun-Yi GUO
;
Yang ZHANG
;
Wei-Hua YAN
;
Ying-Qiu PAN
;
Rui ZHENG
;
Bo-Li LI
;
Wen-Da LUO
Author Information
1. Central Laboratory, Taizhou Hospital, Wenzhou Medical College, Linhai 317000, Zhejiang Province, China. baoguochen@126.com
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Gene Expression Regulation, Neoplastic;
Humans;
Myelodysplastic Syndromes;
metabolism;
pathology;
Signal Transduction;
drug effects;
Sirolimus;
pharmacology;
TOR Serine-Threonine Kinases;
metabolism
- From:
Journal of Experimental Hematology
2010;18(2):300-304
- CountryChina
- Language:Chinese
-
Abstract:
The aim of this study was to investigate the effect of rapamycin on cell growth and apoptosis in the myelodysplastic syndrome (MDS) cell line MUTZ-1 and possible mechanism. MUTZ-1 cells were treated with rapamycin, cell proliferation capability was determined with MTT, protein expression including Annexin V/PI, caspase 3, PTEN, p-Akt, p-mTOR and the cell cycle were analyzed with flow cytometry. The results indicated that the proliferation of MUTZ-1 cells was inhibited by rapamycin in concentration-and time-dependent manners (r=0.67, 0.61, 0.72). After treatment with rapamycin for 24-72 hours, cell count in G0/G1 were significantly higher than that of the control (p<0.01), and this effect showed a time-and concentration-dependency (r=0.94, 0.93, 0.92), the cell cycle was blocked in G0/G1 phase. As compared with control group, the proportion of Annexin V+PI-MUTZ-1 cells and the cellular PTEN levels increased in the treated group dramatically and in time-and dose-dependent manners (p<0.01). To the contrary, level of p-mTOR expression markedly decreased as compared with control group (p<0.05). It is concluded that the rapamycin inhibits the proliferation of MUTZ-1 cells, down-regulates the PTEN/PI3K-Akt/mTOR signaling pathway by interaction with mTOR, which induces the apoptosis of mUTZ-1 cells.
