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. 2016 Dec 7;7:559. doi: 10.3389/fimmu.2016.00559

Figure 1.

Figure 1

Plasma and plasmid-derived hAAT inhibit in vivo development of primary B16-F10 tumors. (A) (i) hAAT+/+ and C57BL/6 mice (n = 10 and 11 per group, respectively) were inoculated i.f.p. with B16-F10 melanoma cells (5 × 104 cells per mouse). Footpad tumor size and representative day-38 footpad tumor photomicrographs. (ii) On day 21 after inoculation of C57BL/6 and hAAT+/+ mice, total tumor RNA was purified, and transcription levels of designated genes were determined. Mean ± SEM, *p < 0.05, **p < 0.01, ***p < 0.001. Unpaired two-tailed Student’s t-test was employed to assess differences between groups at each time point. (iii) C57BL/6 mice (n = 8 per group) were introduced PBS or pEF-hAAT by hydrodynamic tail–vein injection. Six days later, mice were inoculated with B16-F10 cells i.f.p. (5 × 104 cells per mouse). Circulating serum levels of hAAT and tumor size follow-up. Triangle, time of in vivo plasmid introduction. (B) Left: B16-F10 cells (3 × 105 cells in triplicate) were pretreated in vitro with hAAT (0.5 mg/ml) or doxorubicin (60 μM), and cell numbers were counted at indicated time points. Mean ± SEM. Right: B16-F10 cells (3 × 105 cells in triplicate) were pretreated with hAAT (0.5 mg/ml) for 24 h and then stimulated with IFNγ (10 ng/ml) for 24 h. Cells were then stained for MHC class I and analyzed by flow cytometry. Mean ± SEM.