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Papers In Press, published online ahead of print October 17, 2002
Laboratory of Cellular and Molecular Biology, National Institute on Aging, Baltimore, Maryland 21224
Corresponding Author: yusen-liu{at}nih.gov
Arsenic trioxide (As2O3) is highly effective for the treatment of acute promyelocytic leukemia, even in patients unresponsive to all-trans retinoic acid therapy. As2O3 is believed to function primarily by promoting apoptosis, but the underlying molecular mechanisms remain largely unknown. In this report, using cDNA arrays, we have examined the changes in gene expression profiles triggered by clinically achievable doses of As2O3 in acute promyelocytic leukemia NB4 cells. CASPASE-10 expression was found to be potently induced by As2O3. Accordingly, Caspase-10 activity also substantially increased in response to As2O3 treatment. A selective inhibitor of caspase-10, Z-AEVD-FMK, effectively blocked caspase-3 activation and significantly attenuated As2O3-triggered apoptosis. Interestingly, treatment of NB4 cells with As2O3 markedly increased histone H3 phosphorylation at Serine-10, an event that is associated with acetylation of the Lysine-14 residue. Chromatin immunoprecipitation (ChIP) assays revealed that As2O3 potently enhances histone H3 phosphoacetylation at the CASPASE-10 locus. These results suggest that the effect of As2O3 on histone H3 phosphoacetylation at the CASPASE-10 gene may play an important role in the induction of apoptosis and thus contribute to its therapeutic effects on acute promyelocytic leukemia.
J. Biol. Chem, 10.1074/jbc.M207836200
Submitted on August 1, 2002
Revised on October 17, 2002
Accepted on October 17, 2002
Arsenic trioxide promotes histone H3 phosphoacetylation at the chromatin of CASPASE-10 in acute promyelocytic Leukemia cells
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