Extended Data Fig. 9: Pharmacological suppression of STING and ER stress attenuates tumor progression.
From: Non-cell-autonomous cancer progression from chromosomal instability
a–d, Abundance of Gr-MDSCs (a), NK-cells (b), CD8+ T-cells (c), and M2-like macrophages (d) in freshly resected CINhigh 4T1 14-day-old tumors treated with vehicle or AMG44 a PERK inhibitor; bars represent mean values ± s.e.m, * p < 0.05, ** p < 0.01, 2-sided t-test, n = 4 (vehicle) or 7 (AMG44). e, Immunoblots for CHOP and BiP in 4T1 cells with or without tunicamycin treatment in the presence STING inhibitor C-176 or vehicle with β-actin as loading control. f, Relative Ccl2 production levels in vehicle and H-151 treated 4T1 cells; bars represent mean ± SD, **** p < 0.0001, two-sided Welch’s t test, n = 8. g, Gene-set enrichment analysis (GSEA) results showing HALLMARK gene sets that are differentially enriched between vehicle and C-176-treated B16F10 cells, one-sided weighted Smirnov-Kolmogorov test corrected for multiple tests. h, Animal survival upon tail vein inoculation of CT26 or 4T1 cells in BALB/c hosts that were treated with C-176, H151 or a corresponding vehicle control, two-sided log-rank test, n = 15 animals per experimental arm. i, The number of surface lung metastases after tail vein inoculation of CT26 cells; bars represent median values, * p < 0.05, two-sided Mann-Whitney test, n = 12-13 animals per group.
