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. Author manuscript; available in PMC: 2023 Oct 16.
Published in final edited form as: Cell Rep. 2023 Sep 1;42(9):113067. doi: 10.1016/j.celrep.2023.113067

Figure 4. AXL-mediated IL-11 secretion in lung cancer cells and lung stromal fibroblasts activates signaling cascades for pro-tumoral features of macrophages.

Figure 4.

(A and B) IL-11 secretion was attenuated by dubermatinib (40 nmol/L) from A549 lung cancer cells (n = 2) and MRC-5 lung fibroblasts (n = 4). Data are mean ± SD; *p < 0.05, **p < 0.01, ***p < 0.001; Student’s t test for each time point.

(C and D) Kaplan-Meier curves depict overall and disease-free survival probability in TCGA lung adenocarcinoma cohort based on high (Z score > 1) and low (Z score < 1) IL11 expression of lung tumors.

(E) Flow chart of induction of U937-derived macrophages and IL-11 treatment for CyTOF analysis.

(F) AXL and STAT3 correlation scatterplot of U937-derived macrophages.

(G) Violin plots showing the expression levels of AXL and STAT3 without and with IL-11 treatment (25 ng/mL). Data are mean ± SD; ***p < 0.001; Student’s t test.

(H) Western blot analysis of IL-11-activated AXL-STAT3 signaling, i.e., phosphorylation of AXL and STAT3 (pSTAT3) in U937-derived macrophages. The cleavage product, phosphorylated AXL intracellular domain (pAXL-ICD), was observed.

(I and J) Violin plots of expression levels of the seven AXL-STAT3-related markers without and with IL-11 treatment (25 ng/mL). Data are mean ± SD; ***p < 0.001; Student’s t test.

(K) CD86 and CD163 correlation scatterplot of macrophages showing the four subtypes based on mean values of CD86 and CD163 and bar graph of subtype proportions of macrophages without and with IL-11 treatment (25 ng/mL).