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Originally published In Press as doi:10.1074/jbc.M208458200 on December 17, 2002

J. Biol. Chem., Vol. 278, Issue 9, 7422-7430, February 28, 2003
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SW13 Cells Can Transition between Two Distinct Subtypes by Switching Expression of BRG1 and Brm Genes at the Post-transcriptional Level*

Mitsue Yamamichi-Nishina, Taiji Ito, Taketoshi Mizutani, Nobutake Yamamichi, Hirotaka Watanabe, and Hideo IbaDagger

From the Division of Host-Parasite Interaction, Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan

The human adrenal carcinoma cell line, SW13, has been reported to be deficient in both BRG1 and Brm expression and therefore is considered to lack a functional SWI/SNF complex. We found that the original cell line of SW13 is composed of two subtypes, one that expresses neither BRG1 nor Brm (SW13(vim-)) and the another, which does express both (SW13(vim+)). The presence of BRG1 and Brm in SW13 correlates completely with the cellular ability to express such genes as vimentin, collagenase, c-met, and CD44 that were under the control of a transcription factor, AP-1, which was shown previously to require a functional SWI/SNF complex for its transactivating activity. Transient treatment with inhibitors of histone deacetylase induced a stable transition of SW13(vim-) to a cell type indistinguishable from SW13(vim+), suggesting that these two subtypes are epigenetically different. Run-on analysis indicated that, unlike these four genes driven by AP-1, transcription of the BRG1 and Brm genes in SW13(vim-) are initiated at a frequency comparable with SW13(vim+). In both SW13(vim-) and SW13(vim+) cells, the BRG1 and Brm genes were transcribed through the entire gene at a similar efficiency, indicating that their expression was completely suppressed at the post-transcriptional level in SW13(vim-) cells. We would like to propose that SW13 can spontaneously transition between two subtypes by switching expression of BRG1 and Brm at the post-transcriptional level.


* This work was supported in part by a grant-in-aid for scientific research on priority areas from the Ministry of Education, Science, and Culture 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.

Dagger To whom correspondence should be addressed. Tel.: 81-3-5449-5730; Fax: 81-3-5449-5449; E-mail: iba@ims.u-tokyo.ac.jp.


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