Differentiation of human promyelocytic leukemia HL-60 cells induced by proanthocyanidin and its mechanism.
10.7534/j.issn.1009-2137.2013.04.021
- Author:
Zhao-Yang XIE
1
;
Bin-Hua WU
;
Zhi-Gang YANG
;
Xiao-Fang CHEN
;
Qiu-Shen CHEN
Author Information
1. Institute of Medical Laboratorial Examination, Guangdong Medical College, Zhanjiang 524023, Guangdong Province, China (E-mail: pearlxie@163.com).
- Publication Type:Journal Article
- MeSH:
Cell Cycle Checkpoints;
drug effects;
Cell Differentiation;
drug effects;
Cyclin D1;
metabolism;
Cyclin-Dependent Kinase 4;
metabolism;
Cyclin-Dependent Kinase Inhibitor p21;
metabolism;
Gene Expression Regulation, Leukemic;
HL-60 Cells;
Humans;
Proanthocyanidins;
pharmacology
- From:
Journal of Experimental Hematology
2013;21(4):920-925
- CountryChina
- Language:Chinese
-
Abstract:
This study was purposed to investigate the proliferation, differentiation and apoptosis of human promyelocytic leukemia HL-60 cells induced by proanthocyanidin (PAC). HL-60 cells were incubated with 20 mg/L PAC for 24 h, the cell growth was evaluated by CCK-8 assay. the effect of PAC on HL-60 cells was evaluated and the cells morphology was observed by optical microscopy. Expression of CD14 and CD11b, and cell cycle were analyzed by flow cytometry. The results showed that the growth of HL-60 cells was inhibited after treatment with PAC of different concentration in a dose-dependent manner (P < 0.05). 20 mg/L PAC displayed significant effect on HL-60 cells with inhibition ratio (72.3 ± 1.8)% for 24 h. Microscopy displayed that some cells differentiated to relative mature cells after treating for 48 h. Expression of CD14 increased and the expression of CD11b increased a little after treating with 20 mg/L PAC for 24 h, the ratio of cells in G0/G1 phase increased, but the ratio of cells in S phase decreased. The mRNA and protein expression of P21 gene increased, but the protein expression of CDK4 and Cyclin D1 decreased. It is concluded that PAC may inhibit the proliferation of HL-60 cells in vitro, induces the differentiation of HL-60 cells, and arrests the cells in G0/G1 phase. The possible mechanism may be related to up-regulation of P21 gene expression and down-regulation of the protein expression of CDK4 and Cyclin D1.
