Fig. 1: Chemotherapy drugs induce inflammation via the STING pathway.
From: IRE1α translational suppression potentiates STING-dependent chemoresistance in pancreatic cancer

a, b GSEA of upregulated genes in KPC cells treated with cisplatin (Cis, 20 μM) for 24 hours identified enriched gene sets (n = 3). c q-PCR analysis of Il6, Cxcl10, and Ccl5 in KPC cells treated with Cis (20 μM), 5-fluorouracil (5FU, 20 μM), ferroptosis inducer Rsl3 (20 μM), and KRAS inhibitor MRTX1133 (20 μM) for 22 hours (n = 4, representative of two independent biological repeats). d ELISA analysis of IL6 in culture medium from KPC cells treated with Cis (n = 4, representative of two independent biological repeats). e Immunoblot analysis of indicated proteins in KPC cells treated with 20 μM Cis at various time points, representative of three independent biological repeats. f Immunoblot analysis in KPC cells treated with Cis, 5FU, Rsl3, and MRTX1133 for 22 hours, representative of two independent biological repeats. g q-PCR analysis of inflammatory genes in KPC cells treated with Cis alone or in combination with H151 (4 μg/mL, pretreated 1 h prior to Cis treatment) for the indicated time (n = 6, combined from two independent biological repeats). h q-PCR analysis of inflammatory genes in wild-type (WT) or Sting -/- KPC cells treated with or without Cis (n = 4, representative of two independent biological repeats). Immunoblot analysis of STING protein in wild-type (WT) or Sting-/- cells is shown above. The relative intensity of proteins (normalized to β-tubulin or HSP90) or the phosphorylated-to-total protein ratio (p/t) is shown below the blots (e, f). All values are presented as means ± SEM. Statistical significance was determined using an unpaired, two-tailed Student’s t-test, *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001 (c, d, g, h).