Trichostatin A suppresses transformation by the v-myb oncogene in BM2 cells

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Authors

ŠMARDOVÁ Jana NEMAJEROVÁ Alice ŠMARDA Jan JURDIC Pierre KUBALA Lukáš SOUČEK Karel

Year of publication 2003
Type Article in Periodical
Magazine / Source Journal of Hematotherapy Stem Cell Research
MU Faculty or unit

Faculty of Science

Citation
Field Genetics and molecular biology
Keywords myb; histone acetylation; trichostatin A; cyclin D
Description Histone acetylation plays an important role in regulation of transcription and is particularlry relevant to the regulation and pathology of hematopoiesis. In the present study, we examined the contribution of elevated histone acetylation to the differentiation of BM2 monoblasts. Inhibition of the activity of endogenous histone deacetylases by trichostatin A (TSA) resulted in histone hyperacetylation causing cell cycle arrest and differentiation of BM2 cells into macrophage polykaryons. TSA did not affect the level of v-Myb protein in BM2 cells, but it downregulated its transcription activation capability. This suggests that chromatin remodeling can be significantly engaged in regulation of proliferation and differentiation of leukemic cells.
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