Lipoxin A4 Suppresses Lipopolysaccharide-Induced Hela Cell Proliferation and Migration via NF-κB Pathway

Uterine cervical carcinoma (UCC) is one of the most common malignant tumors in females, and UCC has a close relationship with chronic cervicitis. As the endogenous braking signal, lipoxins can regulate anti-inflammation and the resolution of inflammation. We investigated the effect of lipoxin A(4) (LXA(4)) on the proliferation, apoptosis, and migration in lipopolysaccharide (LPS)-stimulated Hela cells. We demonstrated that LXA(4) could significantly suppress p53, cyclin D1 expression, and migration of LPS-stimulated Hela cells via nuclear factor-kappa B (NF-kappa B) pathway, and these effects could be blocked by Boc-2, the specific inhibitor of FPR2/ALX (the receptor of LXA(4)). We presented evidence for a novel role of LXA(4) on the proliferation and migration in LPS-stimulated Hela cells, and FPR2/ALX was involved in the procedures. These results showed that LXA(4) could be a possible candidate for UCC therapy, and blocking the activation of NF-kappa B would be an effective drug target.