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[Cancer Research 61, 7722-7726, November 1, 2001]
© 2001 American Association for Cancer Research

Advances in Brief

Up-Regulation of the Ectodermal-Neural Cortex 1 (ENC1) Gene, a Downstream Target of the ß-Catenin/T-Cell Factor Complex, in Colorectal Carcinomas1

Manabu Fujita, Yoichi Furukawa, Tatsuhiko Tsunoda, Toshihiro Tanaka, Michio Ogawa and Yusuke Nakamura2

Laboratory of Molecular Medicine, Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo 108-8639 [M. F., Y. F., Y. N.]; Department of Surgery II, Kumamoto University School of Medicine, Kumamoto 860-8556 [M. F., M. O.]; SNP Research Center, Riken (Institute of Physical and Chemical Research), Tokyo 108-8639 [T. Ts., T. Ta.], Japan

To clarify the molecular mechanisms of human carcinogenesis associated with abnormal Wnt/wingless signaling, we searched for genes the expression of which was significantly altered by introduction of wild-type AXIN1 into LoVo colon cancer cells. By means of a cDNA microarray, we compared expression profiles of LoVo cells infected with either adenoviruses expressing wild-type AXIN1 (Ad-Axin) or those expressing a control gene (Ad-LacZ). Among the genes showing altered expression, the ectodermal-neural cortex 1 (ENC1) gene was down-regulated in response to Ad-Axin. The promoter activity of ENC1 was elevated ~3-fold by transfection of an activated form of ß-catenin together with wild-type T-cell factor (Tcf)4 in HeLa cells. Semiquantitative reverse transcription-PCR experiments revealed that expression of ENC1 was increased in more than two-thirds of 24 primary colon cancer tissues that we examined compared with corresponding noncancerous mucosae. Introduction of exogenous ENC1 increased the growth rate of HCT116 colon cancer cells in serum-depleted medium. In other experiments, overexpression of ENC1 in HT-29 colon cancer cells suppressed the usual increase of two differentiation markers, in response to treatment with sodium butyrate, a differentiation-inducible agent. These data suggest that ENC1 is regulated by the ß-catenin/Tcf pathway and that its altered expression may contribute to colorectal carcinogenesis by suppressing differentiation of colonic cells.




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Copyright © 2001 by the American Association for Cancer Research.