Abstract
Beta-catenin and Tcf4 are the downstream effectors of the Wnt signaling cascade. In colorectal cancer, mutations in Wnt cascade genes such as APC lead to the inappropriate formation of beta-catenin/Tcf4 complexes. Earlier work has predicted that disruption of the beta-catenin/Tcf4 protein-protein interaction could revert the proliferative phenotype of colorectal cancer cells. In this issue of Cancer Cell, Shivdasani and colleagues have explored high-throughput screening of compound libraries in a search for small molecule inhibitors of the Wnt cascade. Ultimately, such inhibitors could become a novel class of smart anticancer drugs.
MeSH terms
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Adenomatous Polyposis Coli Protein
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Animals
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Antineoplastic Agents / pharmacology
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Colonic Neoplasms / metabolism
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Combinatorial Chemistry Techniques
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Cytoskeletal Proteins / drug effects
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Cytoskeletal Proteins / metabolism*
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DNA-Binding Proteins / drug effects
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DNA-Binding Proteins / metabolism*
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Humans
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Mutation
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Protein Binding* / drug effects
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Protein Binding* / physiology
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Proto-Oncogene Proteins / drug effects
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Proto-Oncogene Proteins / metabolism*
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Signal Transduction / drug effects
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Signal Transduction / physiology
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TCF Transcription Factors
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Trans-Activators / drug effects
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Trans-Activators / metabolism*
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Transcription Factor 7-Like 2 Protein
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Transcription Factors / drug effects
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Transcription Factors / metabolism*
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Wnt Proteins
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Zebrafish Proteins*
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beta Catenin
Substances
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Adenomatous Polyposis Coli Protein
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Antineoplastic Agents
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CTNNB1 protein, human
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Cytoskeletal Proteins
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DNA-Binding Proteins
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Proto-Oncogene Proteins
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TCF Transcription Factors
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TCF7L2 protein, human
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Trans-Activators
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Transcription Factor 7-Like 2 Protein
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Transcription Factors
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Wnt Proteins
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Zebrafish Proteins
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beta Catenin