Regulation of histone acetylation and apoptosis by trichostatin in HL-60 cells / 华中科技大学学报(医学)(英德文版)
Journal of Huazhong University of Science and Technology (Medical Sciences)
; (6): 572-574, 2004.
Article
em En
| WPRIM
| ID: wpr-336975
Biblioteca responsável:
WPRO
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.
Texto completo:
1
Base de dados:
WPRIM
Assunto principal:
Farmacologia
/
Acetilação
/
Química
/
Apoptose
/
Células HL-60
/
Inibidores de Histona Desacetilases
/
Histona Desacetilases
/
Ácidos Hidroxâmicos
/
Antineoplásicos
Limite:
Humans
Idioma:
En
Revista:
Journal of Huazhong University of Science and Technology (Medical Sciences)
Ano de publicação:
2004
Tipo de documento:
Article