Eukaryotic translation initiation factor 3B accelerates the progression of esophageal squamous cell carcinoma by activating β-catenin signaling pathway
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Fengkai Xu1,*, Cheng-Zhi Xu2,*, Jie Gu1,*, Xiaoming Liu3, Ronghua Liu3, Enyu Huang3, Yunfeng Yuan1, Guangyin Zhao1, Jiahao Jiang1, Chen Xu4, Yiwei Chu3, Chunlai Lu1, Di Ge1
1Department of Thoracic Surgery, Zhongshan Hospital, Fudan University, Shanghai, P. R. China
2Department of Otolaryngology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, P. R. China
3Department of Immunology and Key Laboratory of Medical Molecular Virology of MOE/MOH, School of Basic Medical Sciences, Fudan University, Shanghai, P. R. China
4Department of Pathology, Zhongshan Hospital, Fudan University, Shanghai, P. R. China
*These authors contributed equally to this work
Di Ge, email: email@example.com
Chunlai Lu, email: firstname.lastname@example.org
Yiwei Chu, email: email@example.com
Keywords: esophageal squamous cell carcinoma, eukaryotic translation initiation factors 3B, β-catenin signaling pathway
Received: October 22, 2015 Accepted: April 28, 2016 Published: May 30, 2016
Introduction: Esophageal squamous cell carcinoma (ESCC) is one of the most aggressive malignant tumors. Eukaryotic translation initiation factors 3B (EIF3B) is considered to influence tumor proliferation, invasion, apoptosis and cell cycle, which act together to promote the progression of tumors. However, the role of EIF3B in ESCC is unknown. This study aims to explore the clinical and biological role of EIF3B in ESCC.
Results: EIF3B expressions were up-regulated in both ESCC tissues and cell lines. Overexpression of EIF3B was associated with tumor depth, lymph node metastasis and advanced TNM stage. Importantly, patients with high EIF3B expression suffered shorter overall and disease-free survival. Knockdown of EIF3B could inhibit cell proliferation and invasion, promote cell apoptosis, and interfere the cell cycle in vitro. EIF3B-knockdown cells could form smaller subcutaneous tumors in vivo. Finally, we demonstrated EIF3B could activate β-catenin signaling pathway.
Methods: Immunohistochemical staining and Western blot were performed to detect the EIF3B expression in ESCC patient tissues and cell lines. The association between EIF3B expression and patients’ prognosis was analyzed by Kaplan-Meier and Cox regression. Then, CCK-8, colony-formation, Transwell and wound-healing assay were performed to compare the bio-functional change after knockdown of EIF3B. Flow cytometry was applied to analyze the change of cell apoptosis and cycle induced by EIF3B knockdown. Tumor xenograft assay was done to verify the in-vitro results.
Conclusions: EIF3B might serve as a novel marker for predicting prognosis of ESCC patients and as a potential therapeutic target, individually or together with other subunits of EIF3 complex.
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