bml-210 has been researched along with Leukemia* in 1 studies
1 other study(ies) available for bml-210 and Leukemia
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The novel histone deacetylase inhibitor BML-210 exerts growth inhibitory, proapoptotic and differentiation stimulating effects on the human leukemia cell lines.
Histone deacetylase inhibitors have a potent role in the strategy for the treatment of leukemias. BML-210 (N-(2-Aminophenyl)-N' phenyloctanol diamine) is the novel histone deacetylase inhibitor, and its mechanism of action has not been characterized. In this study, we examined the in vitro effects of BML-210 on the human leukemia cell lines (NB4, HL-60, THP-1, and K562). We found that BML-210 inhibits the growth of all cell lines and promotes apoptosis in a dose- and time-dependent manner. BML-210 alone induces HL-60 and K562 cell differentiation (up to 30%) to granulocytes and erythrocytes, respectively, and in combination with differentiation agents - all-trans retinoic acid and hemin, markedly potentates it. Those treatments cause G1 arrest and histone H4 acetylation, affects transcription factor NF-kappaB and Sp1 binding activity to their consensus sequences, the p21 or the FasL promoters, and influences expression of Sp1, NF-kappaB, p21 and FasL. These findings suggest that BML-210 could be a promising antileukemic agent to induce apoptosis and to modulate differentiation through the modulation of histone acetylation and gene expression. Topics: Acetylation; Anilides; Apoptosis; Blotting, Western; Cell Cycle; Cell Differentiation; Cell Line; Cell Line, Tumor; Cell Nucleus; Cell Proliferation; Cytoplasm; Dose-Response Relationship, Drug; Electrophoretic Mobility Shift Assay; Histone Deacetylase Inhibitors; Histone Deacetylases; Histones; HL-60 Cells; Humans; K562 Cells; Leukemia; NF-kappa B; Protein Binding; Time Factors; Transcription Factors; Tretinoin; Tumor Suppressor Protein p53 | 2006 |