Fig. 7

The mechanism graph of the positive feedback loop between GC cells and TAMs. Hypoxia-induced macrophage-derived CXCL8 secretion activated CXCL8- CXCR1/2-JAK/STAT1 signaling pathway and deteriorated the GC malignant phenotype. The transcription factor STAT1 could directly promote IL-10 expression. The latter activated the macrophage IL-10/ NF-κB signaling pathway and induced M2 polarization. The transcription factor NFKB1 directly upregulated CXCL8 expression