Background:Esophageal cancer is one of the worst malignant digestive neoplasms with poor treatment outcomes. Esophagectomy plays an important role and offers a potential curable chance to these patients. However, esophagectomy with radical lymphadenectomy is known as one of the most invasive digestive surgeries which are associated with high morbidity and mortality. The enhanced recovery after surgery (ERAS) protocol is a patient-centered, surgeon-led system combining anesthesia, nursing, nutrition, and psychology, which is designed for reducing complications, promoting recovery, and improving treatment outcomes. This systematic review and meta-analysis is aiming at how beneficial, and to what extent ERAS really will be.Methods:A systematic literature search will be performed through January 2018 using MEDLINE, EMBASE, the Cochrane Central Register of Controlled Trials, and Google Scholar for relevant articles published in any language. Randomized controlled trials, prospective cohort studies, and propensity-matched comparative studies will be included. All meta-analyses will be performed using Review Manager software. The quality of the studies will be evaluated using the guidelines listed in the Cochrane Handbook. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses statements will be followed until the findings of the systematic review and meta-analysis are reported.Results:The results of this systematic review and meta-analysis will be published in a peer-reviewed journal.Conclusion:Our study will draw an objective conclusion of the comparisons between ERAS and conventional care in aspects of perioperative outcomes and provide level I evidences for clinical decision makings.

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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.