FIGURE 2.
NLRP4 regulates type I interferon (IFN) production through the stimulator of IFN genes (STING)‐TANK‐binding kinase 1 (TBK1)‐IFN regulatory factor 3 (IRF3) axis in Lewis lung cancer cells (LLC) cells and retards tumor growth in vivo. A, GFP signals in LLC cells infected with lentivirus containing negative control (NC) or NLRP4 shRNA (NLRP4 KD) (right), or overexpressed NLRP4 gene (NLRP4 OE) (left). Magnification, ×200. Scale bar, 100 μm. B‐D, NLRP4 (B), IFN‐a (C), and IFN‐β (D) mRNA levels were compared between NC and NLRP4 KD‐LLC or NLRP4 OE‐LLC cells. E, Signaling molecules including phospho (p)‐STING, p‐IRF3, and p‐TBK1 between LLC‐NC cells were analyzed among NC‐, NLRP4 KD‐, or NLRP4 OE‐LLC cells. F, G, Proliferative curves of NLRP4 KD‐ and NLRP4 OE‐LLC cells in vitro (F) and in nude mice (G). H, Tumor growth curves in C57BL/6 mice with LLC cell inoculation. The result is the representative of two independent experiments. I, Survival curves of C57BL/6 mice with 0.5 × 106 LLC cells in‐situ implantation. J, Tumor growth curves in C57BL/6 mice with NLRP4 KD‐ and NC‐LLC cell inoculations following anti‐CD8 Ab treatment. P values were calculated using Student’s t test or ANOVA. *P < .05; **P < .01; ****P < .0001. HSP‐90, heat shock protein‐90; OD, optical density; OS, overall survival