RNF219 Promotes Nasopharyngeal Carcinoma Progression by Activating the NF-κB Pathway

In Southeast Asia, the prevalence of nasopharyngeal carcinoma (NPC) is high; however, the molecular mechanism governing the progression of NPC is unclear. The results of the present study revealed upregulation of ring finger protein 219 (RNF219) expression in NPC tissues and cells. Overexpression of RNF219 enhanced NPC cell invasion, migration, and proliferation; whereas knockdown of RNF219 had the opposite effects. Mechanistically, RNF219 activated the nuclear factor kappa B (NF-kappa B) pathway, mainly reflected by increased p65 nuclear translocation, and increased NF-kappa B pathway target gene expression. NF-kappa B pathway inhibition in cells overexpressing RNF219 resulted in reduced invasion, migration, and proliferation, confirming that progression of NPC was promoted by RNF219-mediated NF-kappa B pathway activation. In addition, the expression of RNF219 correlated positively with the activity of the NF-kappa B pathway, verifying that RNF219 regulates the activity of the NF-kappa B pathway in the clinical setting. Our results identified a novel therapeutic target that could promote the development of novel treatments for NPC.

Automated summary

The expression of ring finger protein 219 (RNF219) was upregulated in nasopharyngeal carcinoma (NPC) tissues and cells. RNF219 promoted NPC cell invasion, migration, and proliferation by activating the nuclear factor kappa B (NF-kappa B) pathway. Furthermore, RNF219 expression correlated positively with the activity of the NF-kappa B pathway.