Figure 3.
APTSTAT3-9R inhibits growth of vemurafenib-resistant melanoma tumors and suppresses recruitment of immunosuppressive cells into the TME
(A) Schematic depiction of the experimental design. YUMM1.7R-derived tumors were formed by subcutaneous injection of 3 × 105 cells into C57BL/6 mice. On day 6, each treatment modality was initiated. Both APTSTAT3-9R and APTSCR-9R (10 mg/kg) were injected i.t. every other day, and vemurafenib (20 mg/kg) was injected i.p. daily as indicated. Tumors (n = 5 mice/group) were harvested on day 14 for flow-cytometry analysis. (B) Growth curves of YUMM1.7R-derived melanoma tumors upon treatment with each modality. Tumor size is expressed as mean ± SEM (n = 5 mice/group; ∗∗∗∗p < 0.0001 versus APTSTAT3-9R; two-way ANOVA followed by Tukey’s post hoc test). (C–E) Left: representative contour plots showing the frequency of (C) MDSCs, (D) TAMs, and (E) CD3+CD8+ T cell immune cell populations among live/dead−CD45+ cells in both control and treated groups. Right: quantification of results. Data are presented as means ± SEM (n = 5 mice/group; ∗∗∗∗p < 0.0001, ∗∗∗p < 0.001, ∗∗p < 0.01, ∗p < 0.05; unpaired two-tailed Student’s t test); ns, not significant.
