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. 2019 Nov 20;21(12):1133–1142. doi: 10.1016/j.neo.2019.10.005

Figure 4.

Figure 4

CCL2 mediates ICC-promoting effect of fibroblastic FAP. (A) qRT-PCR analysis of STAT3 regulating inflammatory cytokines particularly CCL2 expression of Ctrl-Fbs, CAFs or FAPkdCAFs. n = 3. (B) ELISA analysis of CCL2 concentrations in the culture of CAFs treated with negative control or fap siRNA. n = 3. (C) qRT-PCR analysis of CCL2 concentrations in the culture of ICC tumor tissues or CAFs. n = 7. (D) Representative flow cytometry analysis of PMN-MDSCs (Ly6G+CD11b+F4/80−), Mo-MDSCs (Ly6C+CD11b+F4/80−) and tumor-associated macrophages (F4/80+CD11b+). (E) Representative flow cytometry analysis of sorted myeloid cells from peripheral blood of ICC patients (CD33+CD14+CD11b+). Transwell assays of MDSC chemotaxis toward supernatants of various fibroblasts with or without CCL2 protein. (F) qRT-PCR analysis of gene expression of proangiogenic factor in MDSCs treated by supernatants of various fibroblasts with or without CCL2. Values are mean ± SEM of three replicate wells from a representative of three experiments. *p < 0.05, **p < 0.01, ***p < 0.001.