Abstract
Precise roles of beta-catenin/TCF pathway involved in esophageal tumorigenesis remain elusive. Here we found STAT3 overexpression in esophageal cancer cells and tissues, and its overexpression in esophageal squamous cell carcinoma (ESCC) tissues correlated with beta-catenin cytoplasmic/nuclear accumulation. A functional TCF binding element was detected in STAT3 promoter which specifically bound to TCF4. Transfected beta-catenin induced STAT3 transcriptional activity dose-dependently, and also enhanced STAT3 mRNA and protein levels. These inductions were specifically abolished by dominant-negative TCF4. These results suggest that STAT3 is a target of beta-catenin/TCF pathway and might participate in esophageal tumorigenesis.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Base Sequence
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Carcinoma, Squamous Cell / metabolism*
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Carcinoma, Squamous Cell / pathology
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Cell Line, Tumor
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Chromatin Immunoprecipitation
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DNA Primers
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Electrophoretic Mobility Shift Assay
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Esophageal Neoplasms / metabolism*
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Esophageal Neoplasms / pathology
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Humans
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Immunohistochemistry
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Promoter Regions, Genetic
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Protein Binding
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RNA, Messenger / genetics
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Reverse Transcriptase Polymerase Chain Reaction
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STAT3 Transcription Factor / genetics
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STAT3 Transcription Factor / metabolism*
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TCF Transcription Factors / metabolism*
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beta Catenin / metabolism*
Substances
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DNA Primers
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RNA, Messenger
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STAT3 Transcription Factor
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STAT3 protein, human
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TCF Transcription Factors
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beta Catenin