Figure S3.
MLH1 deletion induces TREX1 upregulation dependent on the cGAS–STING–IFN–JAK pathway. (A) 4T1 cells (Mlh1−/−day 79) (n = 3/group) were treated by IFNα; before and 6, 9, and 12 h after treatment, cells were collected for Isg15 mRNA detection by RT-qPCR. (B and C) 4T1 cells with or without Mlh1 deficiency (Mlh1−/−; day 85) (n = 3/group) were treated by JAK inhibitor ruxolitinib; after 72 h, cells were collected for Cxcl10 (B) and Isg15 (C) mRNA detection by RT-qPCR. (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 Isg15 mRNA detection by RT-qPCR. (E–H) MC38 cells (n = 3/group) were treated by IFNα or IFNγ; before and 6, 9, and 12 h after treatment, cells were collected for Isg15 (E), Irf1 (F), and Trex1 (G) mRNA detection by RT-qPCR, and Trex1 expression detection by western blot (H). (I) MC38 cells (n = 3/group) were collected for Isg15 mRNA detection by RT-qPCR. (J) 4T1 cells (n = 3/group) (Mlh1−/−; day 98) were collected for Trex1 expression detection by western blot. (K and L) SKBR3 cells (n = 3/group) were infected with vector or shMLH1 lentivirus; after puromycin selection, cells were collected for MLH1 and TREX1 expression detection by western blot (K) and IFNB1 mRNA detection by RT-qPCR (L). (M and N) SKBR3 cells infected with vector or shMLH1 lentivirus (n = 3/group) were treated by cGAS inhibitor RU521 (10 µM); after 72 h, cells were collected for MLH1 and TREX1 expression detection by western blot (M), and IFNB1mRNA detection by RT-qPCR (N). Data are shown as mean ± SEM and are representative of two (A–N) independent experiments. The statistical analysis was performed by unpaired Student’s two-tailed t test in A–G, I, L, and N. NS, not significant, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. Source data are available for this figure: SourceData FS3.

MLH1 deletion induces TREX1 upregulation dependent on the cGAS–STING–IFN–JAK pathway. (A) 4T1 cells (Mlh1−/−day 79) (n = 3/group) were treated by IFNα; before and 6, 9, and 12 h after treatment, cells were collected for Isg15 mRNA detection by RT-qPCR. (B and C) 4T1 cells with or without Mlh1 deficiency (Mlh1−/−; day 85) (n = 3/group) were treated by JAK inhibitor ruxolitinib; after 72 h, cells were collected for Cxcl10 (B) and Isg15 (C) mRNA detection by RT-qPCR. (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 Isg15 mRNA detection by RT-qPCR. (E–H) MC38 cells (n = 3/group) were treated by IFNα or IFNγ; before and 6, 9, and 12 h after treatment, cells were collected for Isg15 (E), Irf1 (F), and Trex1 (G) mRNA detection by RT-qPCR, and Trex1 expression detection by western blot (H). (I) MC38 cells (n = 3/group) were collected for Isg15 mRNA detection by RT-qPCR. (J) 4T1 cells (n = 3/group) (Mlh1−/−; day 98) were collected for Trex1 expression detection by western blot. (K and L) SKBR3 cells (n = 3/group) were infected with vector or shMLH1 lentivirus; after puromycin selection, cells were collected for MLH1 and TREX1 expression detection by western blot (K) and IFNB1 mRNA detection by RT-qPCR (L). (M and N) SKBR3 cells infected with vector or shMLH1 lentivirus (n = 3/group) were treated by cGAS inhibitor RU521 (10 µM); after 72 h, cells were collected for MLH1 and TREX1 expression detection by western blot (M), and IFNB1mRNA detection by RT-qPCR (N). Data are shown as mean ± SEM and are representative of two (A–N) independent experiments. The statistical analysis was performed by unpaired Student’s two-tailed t test in A–G, I, L, and N. NS, not significant, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001. Source data are available for this figure: SourceData FS3.

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