Abstract
The majority of human colorectal cancers have elevated beta-catenin/TCF regulated transcription due to either inactivating mutations of the APC tumor suppressor gene or activating mutations of beta-catenin. Surprisingly, one commonly used colorectal cancer cell line was found to have intact APC and beta-catenin and no demonstrable beta-catenin/TCF regulated transcription. However, this line did possess a truncating mutation in one allele of CDX2, a gene whose inactivation has recently been shown to cause colon tumorigenesis in mice. Expression of CDX2 was found to be induced by restoring expression of wild type APC in a colorectal cancer cell line. These findings raise the intriguing possibility that CDX2 contributes to APC's tumor suppressive effects.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenomatous Polyposis Coli Protein
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Alleles
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CDX2 Transcription Factor
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Colorectal Neoplasms / genetics*
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Colorectal Neoplasms / metabolism
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Cytoskeletal Proteins / genetics
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Cytoskeletal Proteins / metabolism*
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DNA Mutational Analysis
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Gene Expression Regulation, Neoplastic*
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Genes, Tumor Suppressor / genetics
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Genes, Tumor Suppressor / physiology
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Homeodomain Proteins / genetics*
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Homeodomain Proteins / metabolism
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Homeostasis
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Humans
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Mutation*
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Neoplasm Proteins / genetics
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Neoplasm Proteins / metabolism
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Signal Transduction
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Trans-Activators*
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Transcriptional Activation
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Transfection
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Tumor Cells, Cultured
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beta Catenin
Substances
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Adenomatous Polyposis Coli Protein
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CDX2 Transcription Factor
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CTNNB1 protein, human
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Cytoskeletal Proteins
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Homeodomain Proteins
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Neoplasm Proteins
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RNA, Messenger
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Trans-Activators
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beta Catenin