Figure 7

Proposed model for reciprocal crosstalk between GC-MSCs and neutrophils via IL-6–STAT3 axis. GC-MSCs-derived IL-6 activates the STAT3–ERK1/2 signaling cascade in neutrophils, resulting in the prolonged survival and the functional activation of neutrophils. In turn, GC-MSCs-activated neutrophils prompt the metastatic potential of gastric cancer cells and the angiogenic ability of endothelial cells, as well as the transition of normal MSCs to CAFs in tumor stroma