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Originally published In Press as doi:10.1074/jbc.M204938200 on September 26, 2002

J. Biol. Chem., Vol. 277, Issue 49, 47014-47021, December 6, 2002
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Identification of Functional Hypoxia Response Elements in the Promoter Region of the DEC1 and DEC2 Genes*

Kazuko MiyazakiDagger §, Takeshi KawamotoDagger , Keiji Tanimoto, Masahiko Nishiyama, Hiroaki Honda§, and Yukio KatoDagger ||

From the Departments of Dagger  Dental and Medical Biochemistry, Graduate School of Biomedical Sciences, § Developmental Biology, and  Translational Cancer Research, Division of Clinical and Experimental Oncology, Research Institute for Radiation Biology and Medicine, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan

Adaptation to hypoxia is a crucial process both physiologically (i.e. in chondrocytes) and pathologically (i.e. in tumor cells). Previous studies have shown that DEC1, a basic helix-loop-helix transcription factor, is induced by hypoxia in glioma cells (Ivanova, A. V., Ivanov, S. V., Danilkovitch-Miagkova, A., and Lerman, M. I. (2001) J. Biol. Chem. 276, 15306-15315). In the present study, we found that hypoxia or CoCl2 enhanced the mRNA expression of DEC2, as well as DEC1, within 24 h in chondrogenic ATDC5, 293T, and HeLa cells. In luciferase assays, the regions between -524 and -401 in the DEC1 promoter, and between -863 and -258 in the DEC2 promoter, were responsible for the hypoxia- or hypoxia-inducible factor-1alpha (HIF-1alpha )-induced transcription. In these regions, we identified functional hypoxia response elements (HREs) that bound to HIF-1alpha and HIF-1beta . In addition to an HIF-1 binding site consensus sequence, the DEC1 HRE had cAMP response element-like and CACAG sequences, which were also involved in the transcription activation in response to HIF-1alpha . Although the DEC2 HRE did not have a cAMP response element-like or CACAG sequence, it showed a higher affinity for HIF-1 than did the DEC1 HRE. Because DEC1 and DEC2 are directly inducible by HIF-1, these transcription factors may be crucial for the adaptation to hypoxia.

* This work was supported by grants-in-aid for science from the Ministry of Education, Culture, Sport, Science and Technology of Japan.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.

|| To whom correspondence should be addressed. Tel.: 81-82-2575628; Fax: 81-82-2575629; E-mail: ykato@hiroshima-u.ac.jp.

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