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. 2021 Apr 7;22(8):3805. doi: 10.3390/ijms22083805

Figure 2.

Figure 2

Schematic figure representing the interplay between cancer-associated fibroblasts (CAFs) and gastric cancer (GC) cells. As reported in the text, several cells represent sources of CAFs, including bone-marrow-derived cells (BMDCs), local pericytes, and normal fibroblasts, with the latter supporting GC stem cells through the secretion of R-spondin3. CAFs are able to regulate tumor growth and progression through the secretion of several molecules—such as IL-6, CXCL-12, PDGF, EGF, and FGF. Vascular endothelial growth factor A (VEGFA), CXCL12, fibroblast growth factor 2 (FGF2), and platelet-derived growth factor (PDGF) produced by CAFs facilitate the formation of new blood vessels in the TME. CAFs secrete also many chemokines and cytokines, such as CXC chemokine ligand 12 (CXCL12) and transforming growth factor-β (TGFβ), inducing immunosuppression in the TME. Notably enough, a subpopulation of CAFs has been suggested to exert also an inhibitory action on tumor cells. Abbreviations: BMDCs: bone-marrow-derived cells; CAF: cancer-associated fibroblast.