CFTR inhibits the invasion and growth of esophageal cancer cells by inhibiting the expression of NF‐κB

• Published in: Cell biology international 2018-12, Vol.42 (12), p.1680-1687
• Main Authors: Li, Wenjun, Wang, Chaoyang, Peng, Xiaonu, Zhang, Hongwei, Huang, Haibo, Liu, Huimin
• Format: Article
• Language: English
• Subjects: Adenocarcinoma; Adenocarcinoma - genetics; Adenocarcinoma - pathology; Animals; cell invasion; Cell Line, Tumor; Cell migration; Cell Proliferation; CFTR; Conductance; Cystic fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator - genetics; Cystic Fibrosis Transmembrane Conductance Regulator - metabolism; Esophageal cancer; esophageal cancer cells; Esophageal Neoplasms - genetics; Esophageal Neoplasms - pathology; Esophagus; Female; Gene Expression Regulation, Neoplastic; Gene Silencing; Humans; Male; Mice; Mice, Nude; Middle Aged; Neoplasm Invasiveness; NF-kappa B - genetics; NF-kappa B - metabolism; NF‐κB; Protein expression; RNA, Messenger - genetics; RNA, Messenger - metabolism; RNA, Small Interfering - metabolism; Squamous cell carcinoma; Tumor cell lines; tumor growth
• ISSN: 1065-6995; 1095-8355
• DOI: 10.1002/cbin.11069

Our study aimed to explore the function of cystic fibrosis transmembrane conductance regulator (CFTR) in esophageal cancer. Twenty patients with esophageal squamous cell carcinoma (ESCC) and 20 patients with esophageal adenocarcinoma (EA) were enrolled in this study. The levels of CFTR and NF‐κB in tumor tissues and adjacent normal tissues were detected, respectively. The expression of CFTR were detected by qRT‐PCR and Western blot in normal esophageal cell line, esophagus squamous cell, carcinoma cell lines, and EA cell lines, respectively. Effects of CFTR silencing and overexpression on NF‐κB protein expression were detected by Western blot. Transwell assay was performed to detect cell invasion. Mouse tumor model was established and the effect of CFTR inhibitor on tumor growth was examined. The expression of CFTR was downregulated in tumor tissues and cancer cell lines. CFTR silencing promoted the expression of NF‐κB‐p65 and NF‐κB‐p50, and the results of CFTR overexpression were reversed. In addition, CFTR silencing promoted the invasion of cancer cells and tumor growth in mice. Besides that, NF‐κB inhibitor reduced the enhancing effects of CFTR silencing on esophageal cell invasion. We conclude that CFTR inhibits the growth and migration of esophageal cancer cells by downregulating of the NF‐κB protein expression.