promotes cell invasion in gastric cancer by activating the NF-κB signaling pathway.

() overexpression has been reported to be involved in the carcinogenesis and progression of many malignant tumors. However, the role of in the progression of gastric cancer (GC) remains unclear. In this study, we explored whether and how regulates proinflammatory signaling to promote GC cell invasion. Our results showed that knockdown of inhibited GC cell migration and invasion induced by lipopolysaccharide (LPS) stimulation. We also found that both CUL4A and nuclear factor-kappa B (NF-κB) protein expressions were enhanced by LPS stimulation in HGC27 GC cell lines. Furthermore, knockdown of decreased the protein expression of NF-κB and mRNA expression of the downstream genes of the NF-κB pathway, such as matrix metalloproteinase (MMP) 2, MMP9, and interleukin-8. Our immunohistochemistry analysis on 50 GC tissue samples also revealed that CUL4A positively correlated with NF-κB expression. Taken together, our findings suggest that may promote GC cell invasion by regulating the NF-κB signaling pathway and could be considered as a potential therapeutic target in patients with GC.