Abstract
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.
Highlights
Colon cancer is one of the most common malignancies in the world [1, 2]
The expression of FOXN3 was down-regulated in colon cancer
To confirm the results from the analysis of dataset available in the Oncomine database, we examined the mRNA level of FOXN3 in 30 colon cancer tissues and paired non-cancerous adjacent tissues
Summary
Activation of wnt/ beta-catenin signaling is one of the hallmarks of this malignancy [3]. Wnt/beta-catenin signaling has been demonstrated to promote the progression of colon cancer [7]. In the absence of Wnt ligand, Axin, APC, CK1 and GSK3 beta form a destruction complex, which promotes the phosphorylation of beta-catenin at its N-terminal Ser/Thr residues by CK1 and GSK3 beta. Upon the stimulation of wnt ligand, the formation of destruction complex is inhibited, which resulted in the β-catenin stabilization and translocation into nucleus. Aberrant activation of wnt/ beta-catenin signaling promotes the growth, migration and metastasis of colon cancer cells [10, 11]. Targeting the Wnt/beta-catenin signaling pathway is a promising strategy for the treatment of colon cancer
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