Figure 5.

SP promotes the development of tobacco smoke-induced lung cancer in animals

(A) Representative micro-CT image of lungs of an NK-A/J mouse treated with SP and WEB2086 at week 14. A single lung tumor was identified (green circle).

(B–D) micro-CT scan slices highlighted multiple tumors (yellow circles) in a mouse treated with SP at week 14. (B–D) show of micro-CT images of lungs from the same mouse.

(E) 3D reconstruction of the lung tumor shown in (D).

(F) H & E-stained section from the mouse lungs shown in (E) displayed the histological characteristics of lung adenocarcinomas (magnification, ×200).Scale bar, 50 μm.

(G) NNK-mice with SP administration had a significant increase in the number of lung tumors compared with mice without SP treatment or mice treated with SP and WEB2086. Data presented as mean ± SEM (n = 3); ∗p < 0.01 by one-way ANOVA.

(H) Lung tumors of NNK-mice with SP administration were larger than those of NNK-mice without SP treatment or NNK-mice treated with SP and WEB2086. Data presented as mean ± SEM (n = 3); ∗p < 0.01 by one-way ANOVA.

(I) Mice treated with SP displayed a higher level of pro-inflammatory cytokines (IL-1β, IL-4, IL-6, IL-11, IL-12, 17A, IFN-γ, and TGF-β) in their serum compared with mice without SP treatment or treated with both SP and WEB2086. Expression levels of the cytokines in serum of the mice without SP treatment were designated as “1. FirePlex-96 Key Cytokines (Mouse) Immunoassay Panel was used to determine inflammatory cytokines in serum. The results are presented as the mean ± SD of three different experiments with triplicates. Data presented as mean ± SEM (n = 3); ∗p < 0.05 by one-way ANOVA.

(J) Kaplan-Meier survival curves of A/J mice with NNK-induced lung tumors treated with or without SP or SP and WEB2086, ∗p < 0.05, log rank (Mantel-Cox) test.