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. 2021 Mar 10;9(3):e002138. doi: 10.1136/jitc-2020-002138

Figure 4.

Figure 4

Exploration of the mechanism by which IFNGR1 regulates PD-L1 and IDO-1 expression. IHC samples including 30 benign samples, 15 low-level adenocarcinoma, 15 high-level adenocarcinoma, 18 CRPC samples and 16 SCC samples. (A) IHC staining for IFNGR1 in benign, adenocarcinoma, CRPC and SCC tissue samples; the black bars in the IHC image are 200 µm. (B) IHC scores for IFNGR1 expression in different tumors. (C) IFNGR1 expression in N-cad-positive and N-cad-negative tissues. (D) IHC staining for p-IFNGR1 in benign, adenocarcinoma, CRPC and SCC tissue samples; the black bars in the IHC image are 200 µm. (E) IHC scores for p-IFNGR1 levels in different tumors. (F) p-IFNGR1 levels in N-cad-positive and N-cad-negative cases. (G) IHC staining for IFNGR1 in mouse (n=5) tissue samples, the black bars in the IHC view are 200 µm. (H) IHC staining for p-IFNGR1 in mouse (n=5) tissue samples; the black bars in the IHC image are 200 µm. (I) Levels of IFNGR1/p-IFNGR1 in different cell lines. N-cadherin regulates PD-L1 and IDO-1 expression by modulating the JAK/STAT pathway. (J) Expression of PD-L1 and IDO-1 after blockade of the JAK/STAT pathway. (K, L, and M) Activation of the JAK/STAT pathway and PD-L1/IDO-1 expression. (N) Activation of the IFNGR/JAK/STAT pathway after treatment with Kyn. (O) The expression of JAK1/JAK3 in N-cad-overexpressing and N-cad-KO cells. (P) Activation of the IFNGR/JAK/STAT pathway in N-cad-overexpressing and N-cad KO cells treated with IFN-γ. PC3 cells were also used as a positive control. CRPC, castration-resistant prostate cancer; IDO-1, indole amine 2,3-dioxygenase; IFN-γ, interferon gamma; IHC, immunohistochemistry; Kyn, kynurenine; N-cad, N-cadherin; N-cad KO, N-cad knockout; PD-L1, programmed death ligand-1; SCC, small cell neuroendocrine prostate cancer.