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)
J. huazhong univ. sci. tech. med. sci
; (6): 572-4, 2004.
Article
ي En
| WPRIM
| ID: wpr-634189
المكتبة المسؤولة:
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 (P0.05). 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.
النص الكامل:
1
الفهرس:
WPRIM
الموضوع الرئيسي:
Acetylation
/
Apoptosis
/
HL-60 Cells
/
Histone Deacetylases
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Hydroxamic Acids
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Antineoplastic Agents
اللغة:
En
مجلة:
J. huazhong univ. sci. tech. med. sci
السنة:
2004
نوع:
Article