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Nucleic Acids Research Advance Access originally published online on January 9, 2009
Nucleic Acids Research 2009 37(5):1438-1451; doi:10.1093/nar/gkn1082
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Nucleic Acids Research, 2009, Vol. 37, No. 5 1438-1451
© 2009 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Molecular Biology

Differential usage of alternate promoters of the human stress response gene ATF3 in stress response and cancer cells

Keisuke Miyazaki1, Shoko Inoue1, Kazuhiko Yamada1, Masashi Watanabe1, Qin Liu1, Toshiki Watanabe2, Mimi Tamamori Adachi1, Yujiro Tanaka1 and Shigetaka Kitajima1,*

1Department of Biochemical Genetics, Medical Research Institute and Laboratory of Genome Structure and Regulation, School of Biomedical Science, Tokyo Medical and Dental University, Tokyo, 113-8510 and 2Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Kashiwa, 277-8561, Japan

*To whom correspondence should be addressed. Tel: +81 3 5803 5822; Fax: +81 3 5803 0248; Email: kita.bgen{at}mri.tmd.ac.jp

Received October 6, 2008. Revised December 15, 2008. Accepted December 24, 2008.

Stress response gene ATF3 plays a pleiotropic role in determining cell fate in response to mitogenic or stress stimuli. An alternate promoter of the human ATF3 gene (designated P1 in this study) has recently been reported, which is located ~43.5 kb upstream of the previously reported P2 promoter. We showed here that the P1 promoter is highly conserved between human and mouse and is functional in response to various stimuli, whereas the P1 promoter was dominantly induced by serum and the P2 promoter was more efficiently activated in response to TGF-β and oncogenic HRAS. The P1 promoter contains multiple transcriptional start sites, and the different 5'-UTRs markedly affected their translation in response to stress. In human prostate and Hodgkin Reed–Sternberg cancer cells with elevated expression of ATF3, the P1 promoter was constitutively activated and its chromatin structure was modified into active configuration. The differential usage of alternate promoters of the ATF3 gene at both transcriptional and translational level and the modification of chromatin structure may provide a novel mechanism for expressing ATF3 in determining cell fate during stress response and cancer.


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