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Originally published In Press as doi:10.1074/jbc.M206320200 on December 13, 2002

J. Biol. Chem., Vol. 278, Issue 9, 6885-6895, February 28, 2003
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Evidence for a Role of p38 Kinase in Hypoxia-inducible Factor 1-independent Induction of Vascular Endothelial Growth Factor Expression by Sodium Arsenite*

Monique C. A. DuyndamDagger , Saskia T. M. Hulscher, Elsken van der Wall, Herbert M. Pinedo, and Epie Boven

From the Department of Medical Oncology, Vrije Universiteit Medical Center, Amsterdam 1081 HV, The Netherlands

Recently we have demonstrated that sodium arsenite induces the expression of hypoxia-inducible factor 1alpha (HIF-1alpha ) protein and vascular endothelial growth factor (VEGF) in OVCAR-3 human ovarian cancer cells. We now show that arsenic trioxide, an experimental anticancer drug, exerts the same effects. The involvement of phosphatidylinositol 3-kinase and mitogen-activated protein kinase (MAPK) pathways in the effects of sodium arsenite was investigated. By using kinase inhibitors in OVCAR-3 cells, both effects of sodium arsenite were found to be independent of phosphatidylinositol 3-kinase and p44/p42 MAPKS but were attenuated by inhibition of p38 MAPK. A role for p38 in the regulation of HIF-1alpha and VEGF expression was supported further by analysis of activation kinetics. Experiments in mouse fibroblast cell lines, lacking expression of c-Jun N-terminal kinases 1 and 2, suggested that these kinases are not required for induction of HIF-1alpha protein and VEGF mRNA. Unexpectedly, sodium arsenite did not activate a HIF-1-dependent reporter gene in OVCAR-3 cells, indicating that functional HIF-1 was not induced. In agreement with this hypothesis, up-regulation of VEGF mRNA was not reduced in HIF-1alpha -/- mouse fibroblast cell lines. Altogether, these data suggest that not HIF-1, but rather p38, mediates induction of VEGF mRNA expression by sodium arsenite.

* This work was supported by the Walter Bruckerhoff Stiftung.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.

Dagger To whom correspondence should be addressed: Dept. of Medical Oncology, De Boelelaan 1117, Amsterdam 1081 HV, The Netherlands. Tel.: 31-20-444-8327; Fax: 31-20-444-4355; E-mail: mca.duyndam. oncol{at}med.vu.nl.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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