Objective: Toll-like receptors (TLR) have been implicated in tumor progression by affecting the immune response in the tumor microenvironment. Toll like receptors have been described to be present in human cancer cells but the presence and the role of these receptors in the growth and proliferation of human lung cancer cells is not known. We analyzed human lung cancer cells for the presence of TLR-2 receptors and evaluated the proliferation response to a specific TLR-2 agonist.
Methods: Human non-small cell cancer cell (NSCLC) lines A549, (adenocarcinoma) H125 adenosquamous, and H1650 adenocarcinoma (American Type Culture Collection), were cultured using standard techniques. Cells were treated with Pam3CSK4, a specific agonist of TLR2, at doses of 0ug/ml, 5ug/ml, and 10ug/ml for 72 hours. Baseline protein levels of TLR2 were assessed using standard western blotting techniques. Proliferation assays were completed using the MTS assay in response to treatment with the agonist
Results: Protein analysis demonstrated varying but consistently detectable levels of TLR2 protein in each cell line. After treatment with Pam3CSK4 we found that proliferation was significantly promoted in the human lung adenocarcinoma cell lines (p=.03), but not in the adenosquamous cell line (p=0.001).
Conclusion: Toll-like receptor -2 is consistently present and detectable on human lung adenocarcinoma cells. Toll Like receptor -2 activation results in increased proliferation in human lung adenocarcinoma cells and this effect appears to be specific to adenocarcinoma cells. Further study is necessary to elucidate the downstream pathways responsible for the increased proliferation we see in these human lung adenocarcinoma cells, however these findings may suggest TLR-2 to be a possible therapeutic target in human lung cancer.
Citation Format: Patrick Kohtz. Activation of toll-like receptor-2 promotes proliferation in human lung adenocarcinoma cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 4637. doi:10.1158/1538-7445.AM2017-4637