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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Apicidin, a histone deacetylase inhibitor, induces differentiation of HL-60 cells.

The fungal metabolite apicidin (cyclo(N-O-methyl-L-tryptophanyl-L-isoleucinyl-D-pipecolinyl-L-2-amino-8-oxodecanoyl)) inhibited the growth of HL-60 cells in a concentration-dependent manner (100-1000 nM). At higher concentrations (>300 nM), cell death was induced. At 100 nM, it induced hyperacetylation of histone H4 time-dependently, while trichostatin A induced transient hyperacetylation. Apicidin (10-100 nM) increased the cells having nitroblue tetrazolium-reducing activity and expressing CD11b but not CD14 and CD15. The expression of CD11b by apicidin was long lasting, while that by trichostatin A was transient. In K562 cells, apicidin at 10-100 nM did not inhibit cell growth nor express CD11b, CD14 and CD15. Our findings indicate that apicidin inhibits proliferation and induces the early stage of differentiation of HL-60 cells.[1]

References

  1. Apicidin, a histone deacetylase inhibitor, induces differentiation of HL-60 cells. Hong, J., Ishihara, K., Yamaki, K., Hiraizumi, K., Ohno, T., Ahn, J.W., Zee, O., Ohuchi, K. Cancer Lett. (2003) [Pubmed]
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