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. 2022 Oct 18;14(20):5092. doi: 10.3390/cancers14205092

Figure 4.

Figure 4

scL-RB94 inhibits growth of NSCLC tumors via NK cells. (A) Quantitative RT-PCR analysis of ligands associated with NK cell activation (ULPB2, MICA, and MICB) in H292 cells after treatment with scL-RB94 in vitro (N = 6). * p < 0.05, ** p < 0.001, Student’s t test. Flow cytometry analysis of (B) ligands associated with NK cell activation (ULBP1 and ULBP2) in H358 tumors and (C) NK cells infiltrating H292 tumors after scL-RB94 treatment (30 µg/injection/mouse, two injections over 3 days). NK cells were identified by gating CD45+ live cells with NK1.1+NKp46+. * p < 0.05, ** p < 0.001, one-way ANOVA or Student’s t test. In another procedure, athymic mice with H358 tumors were treated with either scL-RB94 or scL-vec (30 µg DNA/injection/mouse, total eight injections over 4 weeks). In one cohort of scL-RB94 treated mice, the NK cells were depleted with anti-NK1.1 antibody, 24 h prior to scL-RB94 treatment (N = 5–8). (D) Flow cytometry analysis of NK cells infiltrating H358 tumors. * p < 0.05, one-way ANOVA. (E) Tumor volume for individual mice was measured and graphed for each group. (F) Quantitative RT-PCR analysis of cytokines (IL-15 and CXCL1) produced by the H358 tumor (human) and host (mouse). ** p < 0.001, Student’s t test.