(A) Inhibition of the increased lung tumors in urethane-treated PDLIM2^mKO mice by STAT3 but not RelA codeletion (n = 5). (B) Increased nuclear STAT3 in AMs of urethane-treated PDLIM2^mKO mice (IF analysis). Scale bar: 20 μm. Nuclear STAT3 in F4/80⁺ cells was analyzed by ImageJ and represented with Pearson’s correlation coefficient (n = 3). (C–E) STAT3 codeletion inhibited (C) the increase of total lung macrophages, the increase of AM ratio, and decrease of IM ratio, and (D and E) the increased lung recruitment and IM/AM differentiation of bone marrow–derived monocytes in urethane-treated PDLIM2^mKO mice (FACS analysis, n ≥ 3). (F–L) In urethane-treated PDLIM2^mKO mice, STAT3 codeletion inhibited the increased Arginase 1 in AMs (F, n = 3, IF analysis), decreased lung CD8⁺ T cell activation (G, n = 3, FACS analysis), increased Vegfa expression in AMs (H, n = 4, qPCR analysis), increased lung tumor angiogenesis (I, n = 3, IHC CD34 staining), increased proliferation and decreased apoptosis of lung tumor cells (J, n = 3, IHC assays), increased CCR2 expression on blood monocytes (K, n = 5, FACS analysis, the gating strategy and representative FACS assays are shown in Supplemental Figure 7), and increased Ccr2 expression in monocytes derived from bone marrow cells (L, n ≥ 3, qPCR). (M) qPCR showing comparable Ccl2 increase in lung tissues of urethane-treated WT and PDLIM2^mKO mice (n ≥ 3; NL, normal lung; TL, tumor-bearing lung). Data shown in A–D, and F–J are representative of 2 independent experiments with similar results. Ordinary 1-way ANOVA (A and C–M) and Student’s t test (2 tailed, unpaired) (B) were performed, and data represent mean ± SEM. *P < 0.05; **P < 0.01; ns, not statistically significant.