Effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of HL-60 cells and its mechanism.
10.7534/j.issn.1009-2137.2014.03.025
- Author:
Xia XIE
1
;
Jie LI
1
;
Rui-Cang WANG
1
;
Rui-Li GENG
1
;
Su-Yun WANG
1
;
Chao WANG
1
;
Xiao-Yun ZHAO
1
;
Hong-Ling HAO
2
Author Information
1. Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China.
2. Department of Hematology, Hebei Provincial People's Hospital, Shijiazhuang 050051, Hebei Province, China. E-mail: h0707@163.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
drug effects;
Celecoxib;
Cell Proliferation;
drug effects;
Cyclin D1;
metabolism;
Cyclin E;
metabolism;
Cyclooxygenase 2;
metabolism;
Cyclooxygenase 2 Inhibitors;
pharmacology;
Gene Expression Regulation, Leukemic;
HL-60 Cells;
Humans;
Oncogene Proteins;
metabolism;
Pyrazoles;
pharmacology;
Sulfonamides;
pharmacology
- From:
Journal of Experimental Hematology
2014;22(3):707-711
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the effect of COX-2 inhibitor celecoxib on proliferation, apoptosis of human acute myeloid leukemia cell line HL-60 and its mechanism. HL-60 cells were cultured with different concentrations of celecoxib for 24 h. Cell proliferation was analyzed by CCK-8 assay, cell apoptosis and cell cycle distribution were detected by flow cytometry. Cyclin D1, cyclin E1 and COX-2 mRNA expressions were determined by RT-PCR. The results showed that after the HL-60 cells were treated with different concentrations of celecoxib for 24 h, the cell growth was significantly inhibited in a dose-dependent manner(r = 0.955), IC50 was 63.037 µmol/L of celecoxib. Celecoxib could effectively induce apoptosis in HL-60 cells also in dose-dependent manner(r = 0.988), blocked the HL-60 cells in the G0/G1 phase. The expression of cyclin D1, cyclin E1 and COX-2 mRNA were downregulated. It is concluded that celecoxib can inhibit the proliferation of HL-60 cells in dose-dependent manner, celecoxib causes cell G0/G1 arrest and induces cell apoptosis possibly through down-regulation of the cyclin D1 and cyclin E1 expression, and down-regulation of COX-2 expression respectively.
