Effect of trichostatin A on histone acetylation level and apoptosis in HL-60 cells.
- Author:
Wei-Kai CHEN
1
;
Yan CHEN
;
Jun-Xia GU
;
Guo-Hui CUI
Author Information
1. Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. chen-weikai@hotmail.com
- Publication Type:Journal Article
- MeSH:
Acetylation;
Apoptosis;
drug effects;
Cell Division;
drug effects;
DNA-Binding Proteins;
HL-60 Cells;
drug effects;
Histone Deacetylases;
physiology;
Histones;
metabolism;
Humans;
Hydroxamic Acids;
pharmacology;
RNA, Messenger;
analysis;
Telomerase;
genetics
- From:
Journal of Experimental Hematology
2004;12(3):324-328
- CountryChina
- Language:Chinese
-
Abstract:
In order to explore the underlying mechanism of high effects and low toxicity of trichostatin A (TSA), the effect of TSA on growth inhibition, histone acetylation level and apoptosis in HL-60 cells and normal human peripheral blood mononuclear cells (NPBMNC) were examined using MTT method, immunocytochemistry technology, and Annexin-V-FITC/PI double staining flow cytometry. The results showed that TSA inhibited growth of HL-60 in time- and dose-dependent manners, and the IC(50) of 36 hours was 100 ng/ml. The apoptosis induction effect of TSA in HL-60 cells was also time- and dose-dependent. Besides, the dose of TSA showing significant apoptotic cytotoxicity in HL-60 cells did not demonstrate apparent apoptosis induction in NPBMNC within definite dose and time range. The histone acetylation level in HL-60 cells and NPBMNC both showed remarkable increase (P < 0.05) after incubated with 100 ng/ml TSA for 4 hours without statistical difference between them is detected (P > 0.05). It is concluded that TSA shows effects of definite and significant growth inhibition and apoptosis induction on HL-60 cells in time- and dose-dependent manners. TSA is able to selectively induce apoptosis in HL-60 cells with low toxicity in NPBMNC at the same time. The mechanism of this selectivity can not be ascribed to the differential regulation of histone acetylation level between HL-60 cells and NPBMNC.
