Author/Authors :
Yan، نويسنده , , Shuang and Zhou، نويسنده , , Cuiqi and Zhang، نويسنده , , Wei and Zhang، نويسنده , , Guo and Zhao، نويسنده , , Xuejian and Yang، نويسنده , , Shangbin and Wang، نويسنده , , Yihua and Lu، نويسنده , , Ning and Zhu، نويسنده , , Hongxia and Xu، نويسنده , , Ningzhi، نويسنده ,
Abstract :
Precise roles of β-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 β-catenin cytoplasmic/nuclear accumulation. A functional TCF binding element was detected in STAT3 promoter which specifically bound to TCF4. Transfected β-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 β-catenin/TCF pathway and might participate in esophageal tumorigenesis.
Keywords :
?-catenin/TCF , ESCC , Target gene , Overexpression , STAT3
