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Originally published In Press as doi:10.1074/jbc.M207986200 on October 8, 2002

J. Biol. Chem., Vol. 277, Issue 50, 48270-48275, December 13, 2002
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Transcriptional Activation of the MUC2 Gene by p53*

Keizou OokawaDagger §, Toshihiro KudoDagger , Shu AizawaDagger , Hiroshi Saito||, and Shigeki TsuchidaDagger

From the Dagger  Second Department of Biochemistry and  First Department of Internal Medicine, Hirosaki University School of Medicine, Zaifucho 5, Hirosaki, Aomori 036-8562, Japan and || Center for Education and Research of Lifelong Learning, Hirosaki University, Bunkyo-cho 1, Hirosaki, Aomori 036-8560, Japan

MUC2 is one of the major components of mucins that provide a protective barrier between epithelial surfaces and the gut lumen. We investigated possible alterations of MUC2 gene expression by p53 and p21Sdi1/Waf1/Cip1 in a human colon cancer cell line, DLD-1, establishing subclones in which a tetracycline-regulatable promoter controls exogenous p53 and p21 expression. MUC2 mRNA more significantly increased in response to p53 than to p21. Unexpectedly, MUC2 expression was also induced in human osteosarcoma cells, U-2OS and Saos-2, by exogenous p53. We next performed a reporter assay to test the direct regulation of MUC2 gene expression by p53. Deletion and mutagenesis of the MUC2 promoter region showed that it contains two sites for transactivation by p53. Furthermore, an electrophoretic mobility shift assay indicated that p53 binds to those elements. We analyzed MUC2 expression in other cell types possessing a functional p53 after exposure to various forms of stress. In MCF7 breast cancer and A427 lung cancer cells, MUC2 expression was increased along with the endogenous p53 level by actinomycin D, UVC, and x-ray, but not in RERF-LC-MS lung cancer cells carrying a mutated p53. These results suggest that p53 directly activates the MUC2 gene in many cell types.

* This work was supported by grants-in-aid for Scientific Research from the Ministry of Education, Science, Sports, and Culture of Japan and by a grant-in-aid from Aomori Medical Foundation.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.: 81-172-39-5019; Fax: 81-172-39-5205; E-mail: kookawa@cc.hirosaki-u.ac.jp.

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