β-Catenin/TCF pathway upregulates STAT3 expression in human esophageal squamous cell carcinoma

被引：111

作者：

Yan, Shuang ^{[1
,2
,3
]}

Zhou, Cuiqi ^{[1
,2
,3
]}

Zhang, Wei ^{[1
,2
,3
]}

Zhang, Guo ^{[1
,2
,3
]}

Zhao, Xuejian ^{[4
]}

Yang, Shangbin ^{[1
,2
,3
]}

Wang, Yihua ^{[1
,2
,3
]}

Lu, Ning

Zhu, Hongxia ^{[1
,2
,3
]}

Xu, Ningzhi ^{[1
,2
,3
]}

机构：

[1] Chinese Acad Med Sci, Inst Canc, Lab Cell & Mol Biol, Beijing 100021, Peoples R China

[2] Chinese Acad Med Sci, Canc Hosp, Beijing 100021, Peoples R China

[3] Peking Union Med Coll, Beijing 100021, Peoples R China

[4] Jilin Univ, Basic Sch Med, Dept Pathophysiol, Changchun 130021, Peoples R China

来源：

CANCER LETTERS | 2008年 / 271卷 / 01期

关键词：

beta-catenin/TCF; STAT3; ESCC; Target gene; Overexpression;

D O I：

10.1016/j.canlet.2008.05.035

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：85 / 97

页数：13

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