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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: Cancer-associated fibroblasts-derived CXCL12 enhances immune escape of bladder cancer through inhibiting P62-mediated autophagic degradation of PDL1

Fig. 8

Blocking CXCL12 inhibited tumor growth and promoted antitumor immunity by decreasing PDL1 expression. (A) Left: Flow cytometry was used to determine the apoptosis rate of T24 cells after indirect co-culture with CD3 + T cells in the presence of CXCL12. Right: values were means ± SD from n = 3 independent experiments. (B) Western blotting showing the effect of murine CXCL12 on CYLD, P62, PDL1 and LC3 in MB49 cells. (C) Diagram of animal experiment procedure for combination therapy. (D) The images of resected tumors in each group. (E) The tumor growth curve of each group that received indicated treatment after inoculation of MB49 cells. Data were presented as means ± SD (n = 6). (F) Tumor weights of each group were shown as means ± SD (n = 6). (G) Flow cytometry analysis of CD8 + T cells percentage in total tumor cells of each group. Data were presented as means ± SD (n = 4). (H) Flow cytometry analysis of CD8 + T cells percentage in CD45 + T cells of each group. Data were presented as means ± SD (n = 4). (I) Flow cytometry analysis of regulatory cells (Tregs) percentage in CD3 + T cells of each group. Data were presented as means ± SD (n = 4). (J) Left: PDL1 expression in IHC of each group. Right: Quantitative IHC analysis of PDL1 staining (n = 4). (K) Western blotting showing the expression of PDL1 in tumor tissues of each group. * P < 0.05; ** P < 0.01; *** P < 0.001; **** P < 0.0001

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