RELT promotes the growth of esophageal squamous cell carcinoma by activating the NF-κB pathway.

The members of the tumor necrosis factor receptor (TNFR) family have been demonstrated to play critical roles in various cancers. However, little is known about the function of the Receptor Expressed in Lymphoid Tissues (RELT) in cancers, which is a member of the TNFR family, especially in the esophageal squamous cell carcinoma (ESCC). In this study, we found that RELT expression was increased in ESCC tissues and was consequently associated with poor overall survival of ESCC patients. Moreover, RELT overexpression was found to promote cell growth, cell cycle progression, and suppressed cell apoptosis in vitro; it also decreased the expression of p27 and caspase 3, and increased the expression of survivin. In addition, RELT contributed to the tumorigenesis of ESCC in vivo. Furthermore, we suggest that RELT may function in the pathogenesis of ESCC by activating the nuclear factor κB (NF-κB) pathway. An inhibitor of NF-κB reversed the RELT-induced malignancy in the ESCC cells. Altogether, our findings identified that RELT served as an oncogene in ESCC through the NF-κB pathway, suggesting that RELT may be developed as a novel biomarker for the diagnosis and treatment of the ESCC.