Fig. 4: NAT10 deficiency induces IFN-I responses in tumor cells. | Nature Communications

Fig. 4: NAT10 deficiency induces IFN-I responses in tumor cells.

From: Inhibition of tumor-intrinsic NAT10 enhances antitumor immunity by triggering type I interferon response via MYC/CDK2/DNMT1 pathway

Fig. 4

A, B GSEA was conducted on DEGs between the WT group and the sgNAT10 group of TC1 (A) and MCA205 (B) tumor cells (n = 3 biologically independent samples). Two positively regulated ‘hallmark’ signatures were identified: interferon-alpha response and interferon-gamma response. The heatmaps of the gene list of ‘hallmark’ signatures are shown on the right. C, D The mRNA expression levels of Ifnb, Stat1, Tlr3, Ddx58, Ccl5, Ccl7, Tap1, and Mx2 in WT and sgNAT10 of TC1 (C) and MCA205 (D) tumor cells were detected by RT-qPCR, with normalization to GAPDH (n = 3 biologically independent samples). From left to right, *P = 0.028; ***P < 0.001; **P = 0.0034; ***P < 0.001; ***P < 0.001; ***P < 0.001; **P = 0.002; ***P < 0.001; ***P < 0.001; *P = 0.0213; ***P < 0.001; ***P < 0.001; ***P < 0.001; ***P < 0.001; respectively. E, F WT or sgNAT10 TC1 (E) and MCA205 (F) tumor cells were subcutaneously transplanted into ifnar-/- C57BL/6 N mice (n = 5 mice per group). From left to right, ***P < 0.001; ***P = 0.0003; ***P < 0.001; **P = 0.0058. The tumor weight and growth were monitored at the indicated time points. Unless specified otherwise, the data are presented as means ± SEM (error bar) and compared using the two-sided Student’s t test. Source data are provided as a Source Data file.

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