TLR4 signaling pathway in mouse Lewis lung cancer cells promotes the expression of TGF-β1 and IL-10 and tumor cells migration

The signaling pathways that trigger tumor cell escape from immune surveillance are not understood completely. Toll-like receptors (TLRs) are considered to be expressed in both immune cells and tumor cells. By detecting TLRs expression in mouse Lewis lung cancer (LLC) before and after co-culture with mouse lymphocytes, the authors concluded that LLC cells constitutively expressed TLR1, TLR2, TLR3, TLR4, TLR5, TLR6 and TLR9. Meanwhile, TLR4 expression in LLC cells was the strongest after co-culture with mouse lymphocytes. To investigate the possible roles of TLR4 signaling pathway in LLC, the concentrations of TGF-beta 1 and IL-10 protein in LLC cells supernatant were detected by ELISA, and the migration of LLC cells were detected by transwell assay after lipopolysaccharide (LPS) stimulation. TLR4 protein expression in LLC cells was also detected after LPS stimulation by FCM. The results indicated that both levels of TGF-beta 1 and IL-10 protein were significantly increased after LPS stimulation and reached to a maximum at 24 h and 10 mu g/mL of LPS. The migrated LLC cells with LPS stimulation were significantly increased and reached to a maximum at 10 mu g/mL of LPS. The expression of TLR4 protein was significantly enhanced after 10 mu g/mL of LPS stimulation. These results suggest that the activation of TLR4 signaling pathway in lung cancer cells may be involved in tumor escape and progression by promoting the expression of TGF-mu 1 and IL-10 and tumor cells migration.