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. 2022 Mar 15;132(6):e147908. doi: 10.1172/JCI147908

Figure 5. Resistance to CTL-mediated killing, regulated by the NANOG axis, is one of the key steps driving the immune-refractory feature of the TME.

Figure 5

(A and B) CT26-no insert or CT26-Nanog cells were transfected with siGFP or siHdac1. (A) Western blot analysis of MCL1 expression. β-Actin was used as an internal loading control. (B) Frequency of apoptotic cells. (C and D) CT26-Nanog cells were transfected with siGFP or siMcl1. (C) Western blot analysis of the expression of MCL1. β-Actin was used as an internal loading control. (D) Frequency of apoptotic cells. (E–H) CT26-Nanog tumor–bearing mice were administered siGFP or siMcl1 with or without anti–PD-1 antibody treatment. (E) Tumor growth curves and (F) changes in tumor volume 17 days after challenge compared with baseline. (G) The frequency of apoptotic cells in the tumors. (H) Quantification of antigen-specific CTLs in spleens from tumor-bearing mice. Ten mice from each group were used for in vivo experiments. Results in the graphs represent 3 independent experiments performed in triplicate. Data represent the mean ± SD. ***P < 0.001, by 1-way ANOVA (B, G, and H) or 2-tailed Student’s t test (D).