C7ORF41 Regulates Inflammation by Inhibiting NF-κB Signaling Pathway

Inflammation is an important biological process for eliciting immune responses against physiological and pathological stimuli. Inflammation must be efficiently regulated to ensure homeostasis in the body. Nuclear factor-kappa B (NF- κ B) signaling is crucial for inflammatory and immune responses. Aberrant activation of NF- κ B signaling leads to development of numerous human diseases. In this study, we investigated the function of chromosome 7 open reading frame 41 (C7ORF41) in NF- κ B signaling during inflammation. C7ORF41 was upregulated in cells stimulated with tumor necrosis factor-alpha or lipopolysaccharide. Moreover, overexpression of C7ORF41 inhibited the activation of NF- κ B and decreased the expression of its downstream target genes. Notably, small hairpin RNA-mediated depletion of C7ORF41 increased the levels of downstream genes and enabled the activation of NF- κ B. In conclusion, C7ORF41 negatively regulated inflammation via NF- κ B signaling and p65 phosphorylation in vitro . These findings may help to diagnose and prognosticate inflammatory conditions and may help develop new strategies for the management of inflammation-related diseases.