Fig. 6

CXCL14-mediated tumor suppression is abrogated by MHC-I knockdown in HNC cells. MOE/E6E7^CXCL14 cells were transduced with shRNAs directed to B2M and enriched for knockdown by FACS sorting for the bottom 10% of MHC-I-expressing cells (MOE/E6E7^CXCL14/shB2M). Flow cytometric analysis of H-2D^b (a) and H-2K^b (b) MHC-I molecules in MOE/E6E7^Vector (gray), MOE/E6E7^CXCL14 (blue), and MOE/E6E7^CXCL14/shB2M (red) cells by flow cytometry. Wild-type B6 mice (n = 10 per group) were s.c. injected with MOE/E6E7^Vector, MOE/E6E7^CXCL14, or MOE/E6E7^CXCL14/shB2M cells (5 × 10⁵ cells/mouse). Tumor volume was measured twice per week (c). Individual growth curves are shown from mice injected with MOE/E6E7^CXCL14 (e) and MOE/E6E7^CXCL14/shB2M (f) cells. Survival rates of mice injected with MOE/E6E7^Vector, MOE/E6E7^CXCL14, and MOE/E6E7^CXCL14/shB2M cells were analyzed as was performed in Fig. 1 (d). Summary model of findings of CXCL14 on peripheral immune cells and on immune gene expression (g). P-value of MOE/E6E7^CXCL14/shB2M cells compared with MOE/E6E7^Vector or MOE/E6E7^CXCL14 cells was determined for tumor growth (c) and survival (d) by two-way ANOVA analysis. ★ represents mice that exhibited tumor growth but had to be excluded due to self-inflicted wounds. *p < 0.01, **p < 0.001. Shown are representative of two independent experiments