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. 2023 Dec 10;24(24):17325. doi: 10.3390/ijms242417325

Figure 2.

Figure 2

iTME as a driving source of EMT in lung cancer. A number of cell types from iTME, including cancer-associated fibroblasts (CAFs), tumor-associated macrophages (TAMs), neutrophils, eosinophils, mast cells, T cells (T helper 17 (Th17) and regulatory T (Tregs) cells), and B cells, induce EMT in lung cancer cells by producing various cytokines. Among them, transforming growth factor (TGF-β) is the most studied, but EMT-inducing activity has also been reported for anti-inflammatory cytokines (interleukin 4 (IL-4), IL-10), pro-inflammatory cytokines (IL-1β, IL-6, IL-17, tumor necrosis factor α (TNF-α)), chemokines (C-C Motif Chemokine Ligand 2 (CCL2), C-X-C Motif Chemokine Ligand 12 (CXCL12), IL-8), prostaglandins D2 and E2 (PGD2, PGE2), and neutrophil extracellular traps (NETs). Along with secretion, some EMT-inducing factors are transported to tumor cells via extracellular vesicles (TGF-β, Snail, microRNA-210 (miR-210)). In addition, lung tumor cells produce PGE2 to stimulate their EMT in an autocrine manner.