Fig. 5
From: Single-cell multi-omics uncovers CPS1 as a breast cancer immune evasion therapeutic target
Enhanced high mitochondrial metabolism leads to a pro-tumorigenic phenotype. (A) KEGG enrichment analysis of 64 MitoScore model genes. (B) scFEA analysis of glucose and lactate metabolic flow differences in MitoScore-positive and negative tumor cells. (C) scmetabolism analysis of metabolic pathway differences in tumor cells. (D) In TCGA-BRCA, hypermetabolic patients phenocopy higher levels of hypoxia and glycolysis. (E) Pattern diagram of high mitochondrial metabolism leading to unfavorable patient prognosis. Left: Molecular mechanisms of MIF-driven tumors, MIF/CXCR4 signaling inhibits T cell killing function, and MIF/HIF-1α promotes glycolysis-dependent cell proliferation. Right side: In patients with high mitochondrial metabolism, enhanced glycolysis and MIF-CXCR4 signaling leads to cancer cell proliferation and immunosuppression, which in turn leads to poor prognosis. Abbreviations: MIF, Macrophage migration inhibitory factor; HIF-1α, hypoxia inducible factor 1 subunit alpha; CXCR4, chemokine receptor 4.
