Effect of valproic acid on apoptosis of leukemia HL-60 cells and expression of h-tert gene.
- Author:
Yi-Qing LI
1
;
Song-Mei YIN
;
Si-Qiong FENG
;
Da-Nian NIE
;
Shuang-Feng XIE
;
Li-Ping MA
;
Xiu-Ju WANG
;
Yu-Dan WU
Author Information
1. Department of Hematology, Sun Yat-Sen University, Guangzhou 510120, Guangdong Province, China.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Caspase 3;
metabolism;
HL-60 Cells;
Humans;
Proto-Oncogene Proteins c-bcl-2;
metabolism;
Telomerase;
metabolism;
Valproic Acid;
pharmacology;
bcl-2-Associated X Protein;
metabolism
- From:
Journal of Experimental Hematology
2010;18(6):1445-1450
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to clarify whether valproic acid (VPA) induces apoptosis of leukemia HL-60 cell line and its possible mechanism. The effect of different concentrations and treatment time of VPA on HL-60 cell proliferation was assayed by cytotoxicity test (CCK-8 method) and fluorescence microscopy, and flow cytometry was used to detect cell apoptosis. The expressions of telomerase subunit h-tert mRNA and apoptosis-related protein as well as caspase-3 activity were detected by real time-quantitative PCR, Western blot and ELISA respectively. The results indicated that VPA inhibited proliferation of HL-60 cells and induced cell apoptosis in a dose dependent manner (r = -0.87). The expressions of anti-apoptotic protein BCL-2 and h-tert mRNA were significantly decreased while the pro-apoptotic protein BAX and caspase-3 activity increased after treatment with VPA. The apoptosis rate of HL-60 cell was negatively correlated with expression of h-tert mRNA. It is concluded that VPA can inhibit leukemia HL-60 cell proliferation and induce apoptosis. The VPA displays anti-leukemia activity possibly through reducing h-tert mRNA and BCL-2 protein expression, increasing BAX expression and activity of caspase-3.
