Research Papers:

Loss of FOXN3 in colon cancer activates beta-catenin/TCF signaling and promotes the growth and migration of cancer cells

Yuedi Dai, Meixing Wang, Haixia Wu, Mi Xiao, Houbao Liu and Dexiang Zhang _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:9783-9793. https://doi.org/10.18632/oncotarget.14189

Metrics: PDF 1686 views  |   HTML 2198 views  |   ?  


Yuedi Dai1, Meixing Wang1, Haixia Wu1, Mi Xiao1, Houbao Liu2,*, Dexiang Zhang3,*

1Department of Medical Oncology, Cancer Hospital of Fudan University, Minhang Branch, Shanghai 200240, China

2General Surgery Department, General Surgery Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China

3General Surgery Department, The Fifth People’s Hospital of Shanghai, Fudan University, Shanghai 200240, China

*These authors have contributed equally to this work

Correspondence to:

Houbao Liu, email: [email protected]

Dexiang Zhang, email: [email protected]

Keywords: FOXN3, colon cancer, beta-catenin/TCF signaling, cell growth and migration

Received: August 20, 2016    Accepted: November 22, 2016    Published: December 26, 2016


Aberrant activation of beta-catenin/TCF is a hallmark of colon cancer. How the functions of nuclear localized beta-catenin are regulated is not fully understood. Here, it was found that FOXN3 (Forkhead box N3) was down-regulated in colon cancer tissues. Forced expression of FOXN3 inhibited the growth, migration and invasion of colon cancer cells, while knocking down the expression of FOXN3 promoted the growth, migration, invasion and metastasis of colon cancer cells. FOXN3 bind to beta-catenin and inhibited beta-catenin/TCF signaling by blocking the interaction between beta-catenin and TCF4. Taken together, these data demonstrated the suppressive roles of FOXN3 in the progression of colon cancer, and indicated that restoring the functions of FOXN3 would be a novel therapeutic strategy for colon cancer.

Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 14189