Fig. 2

Cellular components that influence the tumor microenvironment (TME). Interactions within the TME play a crucial role in accelerating cancer progression. Cancer cells activate the PD-L1/PD-1 axis, leading to T cell exhaustion and impairment of T cell function. In addition, cancer cell-secreted exosomes that carry PD-1 contribute to T cell dysfunction, reducing proliferation and hindering proper function. Natural killer cells counteract tumorigenesis by secreting perforin and granular enzymes. Increased infiltration of Treg cells in the TME secretes TGF-β, inducing fibroblast transformation into cancer-associated fibroblasts (CAFs), promoting extracellular matrix deposition, and causing T cell dysfunction. Myeloid-derived suppressor cells (MDSCs) induce Treg cell formation in the TME through the secretion of PGE-2, IL-10, and TGF-β. Regulatory T cells (Treg), in turn, suppress the function of dendritic cells (DCs) by secreting perforin, leading to DC cell apoptosis. M2-polarized macrophages secrete TGF-β and IL-10, disrupting DC cell function. The interaction between endothelial cells and cancer cells results in angiogenesis, further enhancing cancer progression (created by Biorender.com)