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J. Biol. Chem., Vol. 278, Issue 45, 44178-44187, November 7, 2003

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Reciprocal Inhibition between MyoD and STAT3 in the Regulation of Growth and Differentiation of Myoblasts^*

Yoshihisa Kataoka, Itaru Matsumura, Sachiko Ezoe, Soichi Nakata, Eri Takigawa, Yusuke Sato, Akira Kawasaki, Takashi Yokota¶, Koichi Nakajima||, Armando Felsani**, and Yuzuru Kanakura

From the Department of Hematology/Oncology, Osaka University Graduate School of Medicine, 2-2, Yamada-oka, Suita, Osaka 565-0871, Japan, the ^¶Division of Stem Cell Biology, Department of Cancer Medicine, Graduate School of Medical Science, Kanazawa University, 13-1, Takaramachi, Kanazawa 920-8640, Japan, the ^||Department of Immunology, Osaka City University Medical School, 1-4-3, Asahi-machi, Abeno-Ku, Osaka 545-0051, Japan, and the ^**Instituto di Technologie Biomediche, Viale Marx 43, 00137 Rome, Italy

The development of myoblasts is regulated by various growth factors as well as by intrinsic muscle-specific transcriptional factors. In this study, we analyzed the roles for STAT3 in the growth and differentiation of myoblasts in terms of cell cycle regulation and interaction with MyoD using C2C12 cells. Here we found that STAT3 inhibited myogenic differentiation induced by low serum or MyoD as efficiently as the Ras/mitogen-activated protein kinase cascade. As for this mechanism, we found that STAT3 not only promoted cell cycle progression through the induction of c-myc but also inhibited MyoD activities through direct interaction. STAT3 inhibited not only DNA binding activities of MyoD but also its transcriptional activities. However, the inhibited transcriptional activities were restored by the supplement of p300/CBP and PCAF, suggesting that STAT3 might deprive MyoD of these transcriptional cofactors. In addition, we found that MyoD inhibited DNA binding activities of STAT3, thereby inhibiting STAT3-dependent cell growth and survival of Ba/F3 cells. These results suggest that the development of muscle cells is regulated by the coordination of cytokine signals and intrinsic transcription factors.

Received for publication, May 9, 2003 , and in revised form, August 20, 2003.

^* This work was supported by grants from the Ministry of Education, Science and Culture of Japan; the Mochida Foundation; the Ichiro Kanehara Foundation; the Uehara Memorial Foundation; the Naito Foundation; and the Japan Medical Association. The costs of publication of this article were defrayed in part by the payment of page charges. This 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: Dept. of Hematology and Oncology, Osaka University Graduate School of Medicine, 2-2, Yamada-oka, Suita, Osaka 565-0871, Japan. Tel.: 81-6-6879-3871; Fax: 81-6-6879-3879; E-mail: matumura{at}bldon.med.osaka-u.ac.jp.

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