title: Loss of FOXN3 in colon cancer activates beta-catenin/TCF signaling and promotes the growth and migration of cancer cells.
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.
authors.affiliation: Department of Medical Oncology, Cancer Hospital of Fudan University, Minhang Branch, Shanghai 200240, China.
authors.forename: Yuedi
authors.initials: Y
authors.lastname: Dai
authors.affiliation: Department of Medical Oncology, Cancer Hospital of Fudan University, Minhang Branch, Shanghai 200240, China.
authors.forename: Meixing
authors.initials: M
authors.lastname: Wang
authors.affiliation: Department of Medical Oncology, Cancer Hospital of Fudan University, Minhang Branch, Shanghai 200240, China.
authors.forename: Haixia
authors.initials: H
authors.lastname: Wu
authors.affiliation: Department of Medical Oncology, Cancer Hospital of Fudan University, Minhang Branch, Shanghai 200240, China.
authors.forename: Mi
authors.initials: M
authors.lastname: Xiao
authors.affiliation: General Surgery Department, General Surgery Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China.
authors.forename: Houbao
authors.initials: H
authors.lastname: Liu
authors.affiliation: General Surgery Department, The Fifth People's Hospital of Shanghai, Fudan University, Shanghai 200240, China.
authors.forename: Dexiang
authors.initials: D
authors.lastname: Zhang
mesh_terms: D000818:Animals; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D045744:Cell Line, Tumor; D002465:Cell Movement; D049109:Cell Proliferation; D003110:Colonic Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051858:Forkhead Transcription Factors; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D008819:Mice, Nude; D008822:Mice, Transgenic; D009361:Neoplasm Invasiveness; D009362:Neoplasm Metastasis; D011485:Protein Binding; D012097:Repressor Proteins / Q000235:genetics / Q000378:metabolism*; D015398:Signal Transduction; D013997:Time Factors; D000073940:Transcription Factor 4 / Q000235:genetics / Q000378:metabolism*; D051176:beta Catenin / Q000235:genetics / Q000378:metabolism*
chemical_list: C495270:CTNNB1 protein, human; D018797:Cell Cycle Proteins; C106158:FOXN3 protein, human; D051858:Forkhead Transcription Factors; D012097:Repressor Proteins; C532096:TCF4 protein, human; D000073940:Transcription Factor 4; D051176:beta Catenin
keywords: FOXN3; beta-catenin/TCF signaling; cell growth and migration; colon cancer