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Macrophages are plastic cells that can switch among different states according to bioenergetic or biosynthetic requirements. Our previous work demonstrated that the transcription factor Forkhead Box Protein 1 ( FoxO1 ) plays a pivotal role in regulating the function of macrophages, but the underlying mechanisms are still unclear. Here we identify  FoxO1  as a regulator of macrophage function through metabolic reprogramming. Transcriptomic and proteomic analyses showed that the deficiency of  FoxO1  results in an alternatively activated (M2) phenotype of macrophages, with lower expression of inflammatory response- and migration-associated genes. Using the high content screening and analysis technology, we found that deletion of  FoxO1  in macrophages slows their migration rate and impairs their function to limit tumor cell growth in vitro. Next, we demonstrated that glycolysis is inhibited in  FoxO1 -deficient macrophages, which leads to the observed functional changes and the reduced tumor suppression capability. This prospective study shows that  FoxO1  serves as a bridge between metabolism and macrophage function.

Multi-omics analysis identifies FoxO1 as a regulator of macrophage function through metabolic reprogramming