Abstract
Tumor-associated macrophages (TAMs) are critical in promoting tumor progression and therapeutic resistance. In adapting to metabolic changes in the tumor microenvironment (TME), TAMs reprogram their metabolisms and acquire immunosuppressive and pro-tumor properties. Increased glucose metabolism in TAMs leads to the accumulation of a variety of oncometabolites that exhibit potent tumor-promoting capacity via regulating gene expression and signaling transduction. Glucose uptake also fuels O-GlcNAcylation and other post-translational modifications to promote pro-tumor polarization and function of TAMs. Glucose metabolism coordinates interactions between TAMs and various types of cells in the TME, creating a complex network that facilitates tumor progression. Targeting glucose metabolism represents a promising strategy to switch TAMs from pro-tumor toward anti-tumor function for cancer therapy.
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