Regulation of histone acetylation and apoptosis by trichostatin in HL-60 cells.
- Author:
Xingang LI
1
;
Weikai CHEN
;
Junxia GU
;
Guohui CUI
;
Yan CHEN
Author Information
1. The Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
- Publication Type:Journal Article
- MeSH:
Acetylation;
Antineoplastic Agents;
pharmacology;
Apoptosis;
drug effects;
HL-60 Cells;
Histone Deacetylase Inhibitors;
Histone Deacetylases;
chemistry;
Humans;
Hydroxamic Acids;
pharmacology
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2004;24(6):572-574
- CountryChina
- Language:English
-
Abstract:
In order to examine the strong anticancer action and low toxicity of Trichostatin A (TSA), the effect of TSA was examined on the growth inhibition, acetylation of histone H3 and apoptosis in HL-60 cells by employing MTT, immunocytochemical techniques, and Annexin-V-FITC/ PI assay. Our results showed that TSA could inhibit proliferation of HL- 60 cells in a time- and dose-dependent manner, and the IC50 at the 36th h was 100 ng/ml. The apoptosis-inducing effect of TSA on HL-60 cells was also time- and dose-dependent. But it didn't demonstrate apparent apoptosis induction in NPBMNCs within specific dose and time range. Both of the acetylation of histone H3 in HL-60 cells and NPBMNCs increased significantly (P<0.05) after treated with 100 ng/ml TSA for 4 h. However, there was no significant differences between the two groups (P>0.05). It is concluded that TSA can inhibit growth and induce apoptosis of HL-60 cells in a time- and dose-dependent manner, and is able to selectively induce apoptosis in HL-60 cells but does not respond in NPBMNCs under the same conditions. The difference of TSA between HL-60 cells and NPBMNCs can't be explained by the regulation of histone acetylation.
