Activation of Toll-Like Receptor 2 Promotes Proliferation of Human Lung Adenocarcinoma Cells

Anticancer Res. 2020 Oct;40(10):5361-5369. doi: 10.21873/anticanres.14544.

Abstract

Background/aim: The aim of this study was to evaluate the role of toll-like receptor 2 (TLR2) in the proliferation of human lung cancer cells and identify the signaling pathway that mediates this effect.

Materials and methods: Adenocarcinoma (A549 and H1650) and adenosquamous (H125) cells were treated with increasing doses of Pam3CSK4, a TLR2 agonist. Cell proliferation and NF-ĸB activation were evaluated. NF-ĸB was inhibited prior to treatment with Pam3CSK4 and proliferation was assessed.

Results: TLR2 expression was significantly higher in A549 and H1650 cells compared to H125 cells (p<0.001). TLR2 stimulation induced proliferation in adenocarcinoma cells only and led to a corresponding increase in NF-ĸB activity (p<0.05). Inhibition of NF-ĸB prior to treatment with Pam3CSK4 attenuated this proliferative response.

Conclusion: TLR2 activation induced proliferation of lung adenocarcinoma cells through activation of NF-ĸB. Thus, the TLR2 signaling pathway may be a potential therapeutic target in lung adenocarcinoma.

Keywords: Lung cancer; lung adenocarcinoma; non-small cell lung cancer; nuclear factor-kappa B; proliferation; toll-like receptor 2.

MeSH terms

  • A549 Cells
  • Adenocarcinoma of Lung / drug therapy*
  • Adenocarcinoma of Lung / genetics
  • Adenocarcinoma of Lung / pathology
  • Cell Proliferation / drug effects
  • Gene Expression Regulation, Neoplastic / drug effects
  • Humans
  • Lipopeptides / pharmacology*
  • NF-kappa B / genetics
  • Toll-Like Receptor 2 / agonists
  • Toll-Like Receptor 2 / genetics*

Substances

  • Lipopeptides
  • NF-kappa B
  • Pam(3)CSK(4) peptide
  • TLR2 protein, human
  • Toll-Like Receptor 2