Lipoxin A4 suppresses lipopolysaccharide-induced hela cell proliferation and migration via NF-κB pathway

Inflammation. 2015 Feb;38(1):400-8. doi: 10.1007/s10753-014-0044-6.

Abstract

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 A4 (LXA4) on the proliferation, apoptosis, and migration in lipopolysaccharide (LPS)-stimulated Hela cells. We demonstrated that LXA4 could significantly suppress p53, cyclin D1 expression, and migration of LPS-stimulated Hela cells via nuclear factor-κB (NF-κB) pathway, and these effects could be blocked by Boc-2, the specific inhibitor of FPR2/ALX (the receptor of LXA4). We presented evidence for a novel role of LXA4 on the proliferation and migration in LPS-stimulated Hela cells, and FPR2/ALX was involved in the procedures. These results showed that LXA4 could be a possible candidate for UCC therapy, and blocking the activation of NF-κB would be an effective drug target.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Cell Movement / drug effects*
  • Cell Movement / physiology
  • Cell Proliferation / drug effects*
  • Cell Proliferation / physiology
  • Dose-Response Relationship, Drug
  • Female
  • HeLa Cells
  • Humans
  • Lipopolysaccharides / toxicity*
  • Lipoxins / pharmacology*
  • NF-kappa B / antagonists & inhibitors*
  • NF-kappa B / metabolism
  • Signal Transduction / drug effects*
  • Signal Transduction / physiology

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Lipopolysaccharides
  • Lipoxins
  • NF-kappa B
  • lipoxin A4