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Originally published In Press as doi:10.1074/jbc.M207836200 on October 17, 2002

J. Biol. Chem., Vol. 277, Issue 51, 49504-49510, December 20, 2002
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Arsenic Trioxide Promotes Histone H3 Phosphoacetylation at the Chromatin of CASPASE-10 in Acute Promyelocytic Leukemia Cells*

Ji LiDagger §, Peili ChenDagger §, Natasha SinogeevaDagger §, Myriam GorospeDagger , Robert P. Wersto, Francis J. Chrest, Janice BarnesDagger , and Yusen LiuDagger ||

From the Dagger  Laboratory of Cellular and Molecular Biology and the  Research Resources Branch, NIA Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21224

Arsenic trioxide (As2O3) is highly effective for the treatment of acute promyelocytic leukemia, even in patients who are 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, the 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 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.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ These authors who contributed equally to this work.

|| To whom correspondence should be addressed: Laboratory of Cellular and Molecular Biology, NIA, National Institutes of Health, 5600 Nathan Shock Dr., Baltimore, MD 21224. Tel.: 410-558-8442; Fax: 410-558-8335; E-mail: yusen-liu@nih.gov.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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