Journal
CANCER LETTERS
Volume 271, Issue 1, Pages 85-97Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.canlet.2008.05.035
Keywords
beta-catenin/TCF; STAT3; ESCC; Target gene; Overexpression
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Funding
- National Natural Science Foundation [39925020, 30470674, 30721001]
- National Basic Research Program [2004CB518701]
- 863 Project [2006AA02A403]
- Ministry of Education, PR China [IRT0416, 200500230101]
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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. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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