Table of Contents
ISRN Gastroenterology
Volume 2012, Article ID 207235, 10 pages
Research Article

CCN1 Induces 𝜷 -Catenin Translocation in Esophageal Squamous Cell Carcinoma through Integrin 𝜶 11

1Laboratory of GI Injury and Cancer, VA Long Beach Healthcare System, Long Beach, CA 90822, USA
2Division of Gastroenterology, Department of Medicine, University of California, Irvine, Orange, CA 92868, USA
3Pathology and Laboratory Medicine Service, VA Long Beach Healthcare System, Long Beach, CA 90822, USA
4Diagnostic and Molecular Medicine Service, VA Long Beach Healthcare System, Long Beach, CA 90822, USA

Received 9 March 2012; Accepted 4 April 2012

Academic Editors: G.-T. Huang and F. A. Macrae

Copyright © 2012 Jianyuan Chai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Aims. Nuclear translocation of β-catenin is common in many cancers including esophageal squamous cell carcinoma (ESCC). As a mediator of Wnt signaling pathway, nuclear β-catenin can activate many growth-related genes including CCN1, which in turn can induce β-catenin translocation. CCN1, a matricellular protein, signals through various integrin receptors in a cell-dependent manner to regulate cell adhesion, proliferation, and survival. Its elevation has been reported in ESCC as well as other esophageal abnormalities such as Barrett’s esophagus. The aim of this study is to examine the relationship between CCN1 and β-catenin in ESCC. Methods and Results. The expression and correlation between CCN1 and β-catenin in ESCC tissue were examined through immunohistochemistry and further analyzed in both normal esophageal epithelial cells and ESCC cells through microarray, functional blocking and in situ protein ligation. We found that nuclear translocation of β-catenin in ESCC cells required high level of CCN1 as knockdown of CCN1 in ESCC cells reduced β-catenin expression and translocation. Furthermore, we found that integrin α11 was highly expressed in ESCC tumor tissue and functional blocking integrin α11 diminished CCN1-induced β-catenin elevation and translocation. Conclusions. Integrin α11 mediated the effect of CCN1 on β-catenin in esophageal epithelial cells.