Fig. 7
FFAR2KO lung cancer cells exhibit the enhancement of cancer migration, invasion, and colony formation induced by TLR2 or TLR3. A and B. Ctrl A549 and FFAR2KO A549 cells were treated with vehicle, HKLM, and poly(I:C) for 24 h. Cell migration was assessed by the wound healing assay (A). The results are presented as means ± standard deviation (SD, n = 3 independent experiments (B). *P < 0.05, **P < 0.01, and ***P < 0.001. C and D. Ctrl H1299 and FFAR2KO H1299 cells were treated with vehicle, HKLM, and poly(I:C) for 48 h. Cell migration was assessed by the wound healing assay (C). The results are presented as means ± standard deviation (SD, n = 3 independent experiments (D). *P < 0.05 and **P < 0.01. E and F. Ctrl A549 and FFAR2KO A549 cells were treated with vehicle, HKLM, and poly(I:C), and the cell invasion assay was performed (E). The results are presented as means ± standard deviation (SD, n = 3 independent experiments) (F). **P < 0.01 and ***P < 0.001. G and H. Ctrl H1299 and FFAR2KO H1299 cells were treated with vehicle, HKLM, and poly(I:C), and the cell invasion assay was performed (G). The results are presented as means ± standard deviation (SD, n = 3 independent experiments) (H). **P < 0.01 and ***P < 0.001. I and J. Ctrl A549 and FFAR2KO A549 cells were treated with vehicle, HKLM, and poly(I:C), and the colony-forming assay was performed (I, scale bar: 50 μm). The number of colonies was counted using Adobe Photoshop software, and the results are presented as the mean ± SD of three independent experiments (J, n = 3 plates). *P < 0.05, **P < 0.01, and ***P < 0.001. K and L. Ctrl H1299 and FFAR2KO H1299 cells were treated with vehicle, HKLM, and poly(I:C), and the colony-forming assay was performed (K, scale bar: 50 μm). The number of colonies was counted using Adobe Photoshop software, and the results are presented as the mean ± SD of three independent experiments (L, n = 3 plates). *P < 0.05, *P < 0.01, and ***P < 0.001. M. Schematic model of regulation by FFAR2 in TLR-induced lung cancer progression through the cAMP-AMPK-TAK1 signaling axis for NF-κB activation