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[Cancer Research 52, 5770-5774, October 15, 1992]
© 1992 American Association for Cancer Research

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Cadherin Dysfunction in a Human Cancer Cell Line: Possible Involvement of Loss of {alpha}-Catenin Expression in Reduced Cell-Cell Adhesiveness1

Yutaka Shimoyama, Akira Nagafuchi, Shin Fujita, Masahiro Gotoh, Masatoshi Takeichi, Shoichiro Tsukita and Setsuo Hirohashi2

Pathology Division, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104 [Y. S., S. F., M. G., S. H.]; Department of Surgery, Hiratsuka City Hospital, 1-19-1 Minamihara, Hiratsuka, Kanagawa 254 [Y. S.]; Department of Information Physiology, National Institute for Physiological Sciences, Myodaiji, Okazaki, Aichi 444 [A. N., S. T.]; Department of Biophysics, Faculty of Science, Kyoto University, Kitashirakawa, Sakyo-ku, Kyoto 606 [M. T.], Japan

A human lung cancer cell line, PC 9, was analyzed to elucidate the molecular mechanisms of dysfunction of cadherin-mediated cell-cell adhesion in cancer. Although PC 9 cells strongly expressed E-cadherin at the cell membrane, which was indistinguishable immunochemically from functional E-cadherin, they did not show tight cell-cell adhesion and had reduced E-cadherin-mediated aggregation activity. Immunoprecipitation with E-cadherin and Western blot analysis revealed that PC 9 cells did not express {alpha}-catenin, a cadherin-associated protein, suggesting that this was the cause of the cadherin dysfunction in the cell line. In addition, Northern and Southern blot analyses disclosed homozygous deletion of part of the {alpha}-catenin gene, which might have resulted in the loss of {alpha}-catenin expression in PC 9 cells.

1 This work was supported in part by a Grant-in-Aid from the Ministry of Health and Welfare of Japan for a Comprehensive 10-Year Strategy for Cancer Control.

2 To whom requests for reprints should be addressed.

Received 5/13/92. Accepted 8/ 7/92.




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