Effect of rapamycin on proliferation, apoptosis and regulation of chemokine receptor CXCR4 in RPMI8226 cells.
- Author:
Jia-Jia SHI
1
;
Xiao-Hui JIA
;
Xiao-Hong LI
;
Zhi-Yong CHENG
;
Xiao-Xuan WEI
;
Li-Hong SUN
;
Ze-Lin LIU
Author Information
1. Department of Hematology, Hebei Medical University, Shijiazhuang 050000, Hebei Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Cell Line, Tumor;
Cell Proliferation;
drug effects;
Down-Regulation;
Humans;
Receptors, CXCR4;
metabolism;
Sirolimus;
pharmacology
- From:
Journal of Experimental Hematology
2009;17(2):385-389
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to investigate the effect of rapamycin on proliferation, apoptosis, cell cycle progression and the regulation of chemokine receptor CXCR4 on RPMI8226 cells. Different concentrations of rapamycin were used to treat the multiple myeloma cell line RPMI8226 for different times. The proliferation of the cells was detected by MTT assay; the apoptosis rate and cell cycle were determined by flow cytometry (FCM); apoptosis of cells was observed by inverted microscopy; the cylin D1, CXCR4 and mTOR mRNA expressions were detected by RT-PCR or FQ-PCR after treating RPMI8226 cells with different concentrations of rapamycin. The results indicated that the rapamycin could inhibit the proliferation of RPMI8226 cells and induce their apoptosis. The cell cycle was arrested at the G(0)/G(1) phase. PCR results showed the down-regulation of mTOR, cyclin D1 and mTOR mRNA expressions after treating RPMI8226 cells with different concentrations of rapamycin for 24 hours. It is concluded that the rapamycin significantly inhibits the growth of RPMI8226 cells in a dose-and time-dependent mannes and induce cell apoptosis. Cell cycle arrests at the G(0)/G(1) phase, may be due to the down-regulation of the mTOR and cyclin D1 expressions. In additions, the down-regulation of CXCR4 mRNA expression is correlated with the reduction of adhesion between myeloma cells and stromal cells.
