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J. Biol. Chem., Vol. 277, Issue 1, 854-861, January 4, 2002
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From the c-Myc is one of the most potent regulators of
cell cycle progression in higher eukaryotes. Down-regulation of c-Myc
is a critical event for growth inhibition induced by transforming
growth factor-
c-myc Is a Downstream Target of the Smad
Pathway*,
,,,,
, and**
Department of Biochemistry, The Cancer
Institute of the Japanese Foundation for Cancer Research and Research
for the Future Program, Japan Society for the Promotion of Science,
1-37-1 Kami-ikebukuro, Toshima-ku, Tokyo 170-8455, Japan, the
§ First Department of Surgery, Gunma University School of
Medicine, 3-39-22 Schowa-machi, Maebashi, Gunma 371-8511, Japan, the
¶ Department of Microbiology, Tohoku University School of
Medicine, 2-1 Seiryo-machi Aoba-ku, Sendai 980-8575, Japan, and the
Department of Molecular Pathology, Graduate School of
Medicine, University of Tokyo, Tokyo 113-0033, Japan
(TGF-) and is frequently impaired in cancer cells.
We determined a Smad-responsive element in the c-myc
promoter. This element is a complex of the TGF-1 inhibitory element
(TIE) originally identified in the transin/stromelysin promoter and an
E2F site responsible for transcriptional activation of the
c-myc promoter. Smad3 and E2F-4 directly bound to the
element (TIE/E2F), and substitution of two nucleotides in TIE/E2F
impaired binding of both Smad3 and E2F-4 as well as serum-induced
activation and TGF--induced suppression of the c-myc
promoter activity. Smads bound TIE/E2F within 1 h after
stimulation with TGF-, before the suppression of
c-myc transcription, whereas binding of p130 to TIE/E2F
became augmented later than 12 h. TGF- signaling did not
compete with E2F-4 for binding to TIE/E2F, but reduced p300
co-immunoprecipitating with E2F-4. Therefore, TGF- signaling may
suppress c-myc promoter activity by dissociating p300 from
E2F-4.
*
This study was supported by grants-in-aid for Scientific
Research from the Ministry of Education, Science, Sports, Culture 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.
The on-line version of this article (available at
http://www.jbc.org) contains additional figures.
**
To whom correspondence should be addressed: Dept. of Biochemistry,
The Cancer Institute of the Japanese Foundation for Cancer Research,
1-37-1 Kami-ikebukuro, Toshima-ku, Tokyo 170-8455, Japan. Tel.:
81-3-5394-3866; Fax: 81-3-3918-0342; E-mail:
mit-ind@umin.ac.jp.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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