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Patrick Kohtz
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P3.07 - Immunology and Immunotherapy (ID 723)
- Event: WCLC 2017
- Type: Poster Session with Presenters Present
- Track: Immunology and Immunotherapy
- Presentations: 1
- Moderators:
- Coordinates: 10/18/2017, 09:30 - 16:00, Exhibit Hall (Hall B + C)
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P3.07-005 - Activation of Toll-like Receptor-2 Promotes Proliferation in Human Lung Adenocarcinoma Cells (ID 8482)
09:30 - 09:30 | Presenting Author(s): Patrick Kohtz
- Abstract
Background:
Toll-like receptors (TLR) have been implicated in tumor progression by affecting the immune response in the tumor microenvironment. 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, their proliferation response to a TLR-2 agonist and the role of NFkB in TLR-2 activation.
Method:
Human non-small cell lung cancer (NSCLC) cell lines A549 and 1650 (adenocarcinoma), H1299 metastatic NSCLC and H125 adenosquamous were cultured using standard techniques. Standard Western blotting techniques determined baseline TLR-2 protein levels. Cells were treated with Pam3CSK4, a specific agonist of TLR-2, at doses of 0ug/ml, 5ug/ml, and 10ug/ml for 72 hours, and then the MTS assay was used for proliferation assessment. All cell lines were treated with 10 ug/ml Pam3CSK4 for 48 hours and Western blot analysis determined the level of increase in NFkB phosphorylation. Cells were treated with NFkB inhibitor, Bay11-7082, at doses of 1 uM, 5 uM and 25 uM with concomitant treatment of 10 ug/ml Pam3CSK4 over 5 hours. NFkB inhibition was evaluated by Western blot analysis.
Result:
Protein analysis demonstrated consistently detectable levels of TLR-2 in each cell line (Fig 1a). Proliferation was significantly promoted after Pam3CSK4 treatment in human lung adenocarcinoma cell lines (p=.03), but not in the other cell lines (p<0.05) (Fig 1b). NFkB phosphorylation was increased with TLR2-agonist treatment in adenocarcinoma, decreased in non-adenocarcinoma cells and decreased with specific inhibition of NFkB subunit p65 (Fig1c). Figure 1
Conclusion:
TLR-2 is consistently present and detectable on human lung adenocarcinoma cells. TLR-2 activation results in increased proliferation in human lung adenocarcinoma cells and this effect appears to be specific to adenocarcinoma cells. These effects are dependent on the NFkB signaling pathway. These findings may suggest TLR-2 to be a possible therapeutic target in human lung cancer.
