Abstract: Objective · To investigate the regulatory effects of inflammatory signaling pathway on the of G protein-coupled receptor class C group 5 member A (GPRC5A). Methods · Nuclear factor κB (NF-κB)-driven luciferase mice were intraperitoneally injected with lipopolysaccharide (LPS) to evaluate the activation of NF-κB in lungs. GPRC5A in lungs was assessedWestern blotting in the C57BL/6J mice injected with LPS. In vitro tests, human lung tumor cell lines Calu-1 and H322, and human embryonic kidney cell line HEK293T were administered with tumor necrosis factor α (TNF-α) or transfected with p65 plasmid; Western blotting, RT-PCR, luciferase reporter gene experiment and immunofluorescence assay were used to analyze the effect of inflammation on GPRC5A . Results · Intraperitoneal injection of LPS induced activation of NF-κB pathway in lung tissues, which suppressed the of GPRC5A in mice lungs. In Calu-1 cells, TNF-α treatment greatly suppressed the of GPRC5A protein and mRNA. In HEK293T cells, transfection of p65 subunit of NF-κB suppressed the of GPRC5A promoter-driven luciferase reporter. The H322 cells transfected with green fluorescent protein-p65 almost did not express GPRC5A. Conclusion · NF-κB pathway acts at the promoter of GPRC5A and suppresses its mRNA and protein .

Key words: G protein-coupled receptor class C group 5 member A (GPRC5A), lung tumor, inflammation, nuclear factor &, kappa, B (NF-&, kappa, B), tumor necrosis factor &, alpha, (TNF-&, alpha, )