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

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-kappa B activation were evaluated. NF-kappa B 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-kappa B activity (p<0.05). Inhibition of NF-kappa B prior to treatment with Pam3CSK4 attenuated this proliferative response. Conclusion: TLR2 activation induced proliferation of lung adenocarcinoma cells through activation of NF-kappa B. Thus, the TLR2 signaling pathway may be a potential therapeutic target in lung adenocarcinoma.