Fig. 9: Molecular mechanisms of GC growth and metastasis involving CAFs and TREM2+LAM. | Communications Biology

Fig. 9: Molecular mechanisms of GC growth and metastasis involving CAFs and TREM2+LAM.

From: Defining gastric cancer ecology: the crucial roles of TREM2+ macrophages and fibroblasts in tumor microenvironments

Fig. 9

The tumor microenvironment (TME) is illustrated as a dynamic interface involving cancer-associated fibroblasts (CAFs), lipid-associated macrophages (TREM2+LAM), CD8+ T cells, and tumor cells. CAFs secrete CXCL12, which interacts with CXCR4 expressed on TREM2+LAM, promoting their immunosuppressive phenotype via lipid metabolism-related factors (FABP4/5). TREM2+LAM express CD206 and inhibit CD8+ T cell activity by reducing TNF-α secretion, creating an immunosuppressive microenvironment. This interaction enhances tumor proliferation, migration, invasion, and resistance to apoptosis. Metastatic dissemination to secondary sites, such as the lungs, is facilitated by these TME-driven processes. The diagram emphasizes the CXCL12-CXCR4 axis as a critical mediator in CAF and TREM2+LAM crosstalk.

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