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Papers In Press, published online ahead of print December 18, 2001
J. Biol. Chem, 10.1074/jbc.M111255200
Submitted on November 27, 2001
Revised on December 13, 2001
Accepted on December 17, 2001

Activation of the wnt pathway interferes with SRE-driven transcription of immediate early genes

David A. Tice, Irina Soloviev, and Paul Polakis

Molecular Oncology, Genentech, Inc., South San Francisco, CA 94080

Corresponding Author: ppolakis{at}gene.com

Mutational activation of the Wnt signaling pathway is a common early event in colorectal tumorigenesis and the identification of target genes regulated by this pathway will provide a better understanding of tumor progression. Gene expression profiling on oligonucleotide microarrays revealed reduced expression of the immediate early genes fos and fosB following stimulation of cells by Wnt-1. Further analysis demonstrated that serum or 12-O-tetradecanoylphorbol 13-acetate (TPA) activation of several immediate early genes, including fos, fosB, junB, and egr1, was inhibited by Wnt signaling. Wnt signaling inhibited transcriptional activation driven by the serum response element (SRE) without altering the activation of the extracellular signal-regulated kinase (ERK) cascade or ternary complex formation at the fos SRE promoter. The Wnt-mediated repression of c-Fos, FosB, and JunB expression was consistent with a decrease in their binding to an AP-1 promoter element and decreased target gene transcription. The expression of fos, fosB, junB and egr1 was also repressed in human colon tumors relative to patient matched normal tissue. By contrast, the fos family member fra-1 was upregulated in the human colon tumors suggesting a compensatory mechanism for the reduction in fos and fosB expression. The results indicate that Wnt signaling can repress the expression of certain immediate early genes and that this effect is consistent with changes in gene expression observed in human colorectal tumors.


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