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Originally published In Press as doi:10.1074/jbc.C100359200 on August 1, 2001

J. Biol. Chem., Vol. 276, Issue 38, 35239-35242, September 21, 2001
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ACCELERATED PUBLICATION
The Epidermal Growth Factor Receptor Regulates Interaction of the Human DF3/MUC1 Carcinoma Antigen with c-Src and beta -Catenin*

Yongqing LiDagger , Jian RenDagger , Wei-hsuan Yu§, Quan Li, Hiroaki Kuwahara, Li Yin, Kermit L. Carraway III, and Donald Kufe||

From the Dana-Farber Cancer Institute, Harvard Medical School, Boston, Massachusetts 02115, the § Division of New Born Medicine, Children's Hospital, Harvard Medical School, Boston, Massachusetts 02115, and the  Department of Biological Chemistry and University of California Davis Cancer Center, University of California at Davis, Sacramento, California 95817

The DF3/MUC1 mucin-like, transmembrane glycoprotein is aberrantly overexpressed in most human carcinomas. The MUC1 cytoplasmic domain interacts with the c-Src tyrosine kinase and thereby increases binding of MUC1 and beta -catenin. In the present work, coimmunoprecipitation studies demonstrate that MUC1 associates constitutively with the epidermal growth factor receptor (EGF-R) in human ZR-75-1 breast carcinoma cells. Immunofluorescence studies show that EGF-R and MUC1 associate at the cell membrane. We also show that the activated EGF-R phosphorylates the MUC1 cytoplasmic tail on tyrosine at a YEKV motif that functions as a binding site for the c-Src SH2 domain. The results demonstrate that EGF-R-mediated phosphorylation of MUC1 induces binding of MUC1 to c-Src in cells. Moreover, in vitro and in vivo studies demonstrate that EGF-R increases binding of MUC1 and beta -catenin. These findings support a novel role for EGF-R in regulating interactions of MUC1 with c-Src and beta -catenin.

* This work was supported by Grant CA87421 awarded by the NCI.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 These authors contributed equally to this work.

|| To whom correspondence should be addressed: Adult Oncology, Dana-Farber Cancer Institute, 44 Binney St., Boston, MA 02115. Tel.: 617-632-3141; Fax: 617-632-2934; E-mail: donald_kufe@dfci.harvard.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.


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