Extended Data Fig. 8: Consequences of IL-1β signaling in tumor cells.
From: IL-1β+ macrophages fuel pathogenic inflammation in pancreatic cancer
a, Volcano plot (left) of genes up-regulated (red) or down-regulated (blue) in PDAC (KPC) cells treated with IL-1β for 24 h (UT n = 3, IL-1β n = 2). Selected genes are highlighted. Quantification (ELISA) of the indicated cytokines (mean ± SD, n = 3, unpaired two-tailed student’s t test, middle) or PGE2 (n = 7, paired two-tailed student’s t test, right) in the supernatant of PDAC cells (KPC) cells treated with IL-1β 24 h. *p < 0.5, **p < 0.01, ****p < 0.0001. b, Growth curves (mean±SEM) of PDAC cells (subcutaneous KPC) in wild-type and Ccr2−/− mice (left, n = 5/group) or in wild-type mice treated with an anti-CSF-1 antibody (αCSF-1, n = 8) or isotype control (IgG, n = 10). ****p < 0.0001 (two-way ANOVA). c, GSEA (GO BP) on genes ranked by log2FC between PDAC cells (KPC) treated with IL-1β versus untreated controls. NES, Normalized Enrichment Score. d, Scheme of the experiment (left) and expression of Il1b (RT-qPCR, mean±SD) in BMDMs treated for 2 h with tumor-conditioned media (TCM) of mouse PDAC cells (KPC) from the following conditions: untreated (KPCUT) or treated for 24 h with a COX-2 inhibitor (KPCCOX2i), IL-1β (KPCIL-1β), IL-1β + COX-2 inhibitor (KPCIL-1β+COX2i). A control condition of BMDMs stimulated with vehicle or COX-2 inhibitor (COX2i) is shown. Isotype control or an anti-TNF-α antibody (αTNF-α) groups were included for each condition (n = 3). *p < 0.05 **p < 0.01 ***p < 0.001 (two-way ANOVA).