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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Enhanced histone H3 acetylation of the PD-L1 promoter via the COP1/c-Jun/HDAC3 axis is required for PD-L1 expression in drug-resistant cancer cells

Fig. 3

JNK/c-Jun signaling activation is enhanced and mediates the PD-L1 increase in drug-resistant A549/CDDP, MCF7/ADR and HepG2/ADR cells. Drug-resistant cancer cells and their parental cancer cells were used to detect JNK/c-Jun signaling activation. a p-JNK, JNK, p-c-Jun, c-Jun and PD-L1 expression was detected by western blotting, and b c-Jun and p-c-Jun expression in the nuclear and cytoplasmic fractions of drug-resistant cancer cells and their parental cancer cells was detected by western blotting. Representative immunofluorescence images of p-c-Jun expression and its subcellular location in drug-resistant cancer cells and their parental cancer cells are shown (c), and the average fluorescence intensity was measured and compared (d). Images were taken at × 20 magnification, and the specified fields were taken at × 40 magnification. Parental cancer cells were treated with the JNK agonist anisomycin (Aniso, 10 μM) for 48 h (e), while drug-resistant cancer cells were treated with the JNK inhibitor SP6000125 (SP, 10 μM) for 48 h (f). PD-L1 expression was then determined by western blotting. All experiments were performed independently in triplicate. *P ≤ 0.05, **P ≤ 0.01, ***P ≤ 0.001

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