dMMR tumors upregulated TREX1 in an intrinsic cGAS–STING–IFN-dependent manner. (A and B) 4T1 with or without Mlh1 (Mlh1^−/−; day 79) cells (n = 3/group) were treated by IFNα; before and 6, 9, and 12 h after treatment, cells were collected for Trex1 expression detection by western blot (A) and RT-qPCR (B). (C) 4T1 cells with or without Mlh1 (Mlh1^−/−; day 85) deficiency (n = 3/group) were treated by JAK inhibitor ruxolitinib; after 72 h, cells were collected for Trex1 expression detection by RT-qPCR and western blot. (D) MC38 cells with or without Ifnar1 deficiency (n = 3/group) were treated by IFNα; before and 4, 8, and 12 h after treatment, cells were collected for Trex1 expression detection by RT-qPCR and western blot. (E) MC38 cells (n = 3/group) were collected for Trex1 expression detection by RT-qPCR and western blot. (F) MC38 cells were collected for Trex1 expression detection by western blot. (G and H) 4T1 (Mlh1^−/−; day 98) cells (n = 3/group) were collected for Trex1 (G) and Isg15 (H) mRNA detection by RT-qPCR. Data are shown as mean ± SEM and are representative of two (A–H) independent experiments. The statistical analysis was performed by unpaired Student’s two-tailed t test in B–E, G, and H. NS, not significant, ***P < 0.001, and ****P < 0.0001. Source data are available for this figure: SourceData F3.