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Role of a BCL9-Related ß-Catenin-Binding Protein, B9L, in Tumorigenesis Induced by Aberrant Activation of Wnt Signaling

¹ Laboratory of Molecular and Genetic Information, Institute for Molecular and Cellular Biosciences and ² Human Genome Center, Institute of Medical Science, The University of Tokyo, Tokyo, Japan; ³ Second Department of Surgery, Gunma University School of Medicine, Gunma, Japan; ⁴ OTSUKA GEN Research Institute, Otsuka Pharmaceutical Co., Ltd., Tokushima, Japan; and ⁵ Department of Molecular Cell Biology, Medical Research Institute, Tokyo Medical and Dental University, Tokyo, Japan

Wnt signaling plays a crucial role in a number of developmental processes and in tumorigenesis. ß-Catenin is stabilized by Wnt signaling and associates with the TCF/LEF family of transcription factors, thereby activating transcription of Wnt target genes. Constitutive activation of ß-catenin-TCF–mediated transcription resulting from mutations in adenomatous polyposis coli (APC), ß-catenin, or Axin is believed to be a critical step in tumorigenesis among divergent types of cancers. Here we show that the transactivation potential of the ß-catenin-TCF complex is enhanced by its interaction with a BCL9-like protein, B9L, in addition to BCL9. We found that B9L is required for enhanced ß-catenin-TCF–mediated transcription in colorectal tumor cells and for ß-catenin–induced transformation of RK3E cells. Furthermore, expression of B9L was aberrantly elevated in about 43% of colorectal tumors, relative to the corresponding noncancerous tissues. These results suggest that B9L plays an important role in tumorigenesis induced by aberrant activation of Wnt signaling.

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