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The intricate network of the CXCL8-CXCR1/2 axis in TME. CXCL8 binding to CXCR1/2 activates G-protein-mediated signaling cascades in cancer cell. CXCR1/2 activation leads to the dissociation of the Gα subunit from the Gβγ subunits. The signal of Gβγ subunits activate kinase to enhance angiogenesis, proliferation, and invasion. Cancer cell autocrine CXCL8 to recruit MDSCs or neutrophil to TME. Dysbiosis or inflammation affects myeloid cell recruitment through the gut–brain axis.
