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. 2020 Aug 14;17(8):1978–1997. doi: 10.1080/15548627.2020.1805214

Figure 8.

Figure 8.

In vivo targeting of autophagy in immune-refractory tumor cells potentiates the antitumor effects of CTL in a preclinical cancer model. (A) Schematic of the therapy regimen in mice implanted with MDA-MB231 P3 cells. (B) Tumor growth, (C) mass (at 21 d after challenge), and (D) survival of mice inoculated with MDA-MB231 P3 treated with the indicated reagents. (E) Western blot analysis of LC3B, p-EGFR, EGFR, p-AKT1, AKT1, MCL1, and CCNA1 protein in mice administered siGFP or siLC3B #1, with or without adoptive transfer of MLANA-specific CTLs. (F) The proliferation index of cells inside the tumor, as measured by the mean fluorescence intensity of MKI67 staining. (G) Flow-cytometric analysis of the frequency of CFSE-labeled MLANA-specific CTL in the tumors of mice with or without adoptive transfer of CFSE-labeled MLANA-specific CTL. (H) The frequency of apoptotic cells in the tumors of siGFP- or siLC3B #1-treated mice, with or without adoptive transfer of MLANA-specific CTL. For the in vivo experiments, five mice from each group were used. *p < 0.01 and **p < 0.001, by two-way ANOVA (B), one-way ANOVA (C, F, and H), or log-rank test (D) or 2-tailed Student’s t-test (G). The data represent the mean ± SD