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

Apicidin, a histone deacetylase inhibitor, inhibits proliferation of tumor cells via induction of p21WAF1/ Cip1 and gelsolin.

Apicidin [cyclo(N-O-methyl-L-tryptophanyl-L-isoleucinyl-D-pipecolinyl -L-2-amino-8-oxodecanoyl)] is a fungal metabolite shown to exhibit antiparasitic activity by the inhibition of histone deacetylase ( HDAC). In this study, we evaluated apicidin as a potential antiproliferative agent. Apicidin showed a broad spectrum of antiproliferative activity against various cancer cell lines, although with differential sensitivity. The antiproliferative activity of apicidin on HeLa cells was accompanied by morphological changes, cell cycle arrest at G1 phase, and accumulation of hyperacetylated histone H4 in vivo as well as inhibition of partially purified HDAC in vitro. In addition, apicidin induced selective changes in the expression of p21WAF1/ Cip1 and gelsolin, which control the cell cycle and cell morphology, respectively. Consistent with increased induction of p21WAF1/ Cip1, phosphorylation of Rb protein was markedly decreased, indicating the inhibition of cyclin-dependent kinases, which became bound to p21WAF1/ Cip1. The effects of apicidin on cell morphology, expression of gelsolin, and HDAC1 activity in vivo and in vitro appeared to be irreversible, because withdrawal of apicidin did not reverse those effects, whereas the induction of p21WAF1/ Cip1 by apicidin was reversible. Taken together, the results suggest that induction of histone hyperacetylation by apicidin is responsible for the antiproliferative activity through selective induction of genes that play important roles in the cell cycle and cell morphology.[1]


  1. Apicidin, a histone deacetylase inhibitor, inhibits proliferation of tumor cells via induction of p21WAF1/Cip1 and gelsolin. Han, J.W., Ahn, S.H., Park, S.H., Wang, S.Y., Bae, G.U., Seo, D.W., Kwon, H.K., Hong, S., Lee, H.Y., Lee, Y.W., Lee, H.W. Cancer Res. (2000) [Pubmed]
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