Fig. 3: Increased inflammatory response and decreased OXPHOS and RP expression in PTGER4^hi myeloid cells in human tumors.

a UMAP projection of TIM subclusters (left) and signature gene expression in the TIM subclusters (right). b UMAP plots displaying PTGER2 (upper left) and PTGER4 (upper right) expression on TIM subclusters and a dot plot illustrating the fraction of TIM subcluster cells expressing genes involved in PGE biosynthesis and its receptors (bottom). c Grouping of PTGER4-expressing total TIM cells based on PTGER4 expression levels. d Distribution of upregulated and downregulated genes in PTGER4^hi compared to PTGER4^lo total TIM cells (left) and PTGER4^hi compared to PTGER4^lo TIM_C1QA cells (right). e GSEA of DEGs between PTGER4^hi and PTGER4^lo total TIM cells for the following pathways: HALLMARK_TNFA_SIGNALING_VIA_NFKB, HALLMARK_INFLAMMATORY_RESPONSE, HALLMARK_MYC_TARGETS_V1 and HALLMARK_OXIDATIVE_PHOSPHORYLATION. P-values were calculated using adaptive multilevel splitting Monte Carlo approach and adjusted via Benjamini–Hochberg procedure. f Heatmaps showing log₂ fold change in gene expression between PTGER4^hi and PTGER4^lo in total TIM cluster cells (left) and TIM_C1QA subcluster cells (right). The representative genes in cell activation, NFκB components, OXPHOS and RP in PTGER4^hi compared to PTGER4^lo cells are shown. The samples with less than 3 cells per group were excluded from analyses in (d) and (f). Source data are provided as a Source Data file.