CYC1 (cytochrome c1) is a catalytic core subunit of mitochondrial respiratory chain complex III (ubiquinol-cytochrome c oxidoreductase) that transfers electrons from the Rieske iron-sulfur cluster to cytochrome c [UniProt]. This electron transfer is essential for the Q cycle, which couples redox reactions to proton translocation across the inner mitochondrial membrane, driving the electrochemical gradient required for ATP synthesis [UniProt]. CYC1 contains a c-type heme and participates in the coordinated function of complexes II-IV to transfer electrons from NADH and succinate to oxygen [UniProt]. Beyond canonical respiration, CYC1 exhibits unexpected metabolic and regulatory roles. CYC1 overexpression in osteosarcoma tissues correlates with tumor progression, and its silencing reduces complex III activity, sensitizing cells to TRAIL-induced apoptosis via mitochondrial-dependent pathways 1. Similarly, elevated CYC1 in breast cancer promotes metastasis by suppressing AMPK activation and enhancing ATP production 2. In Candida albicans, lysine-79 methylation of cytochrome c (Cyc1) regulates fungal virulence by modulating PKA signaling and controlling hyphal morphogenesis 3. Clinically, CYC1 dysregulation associates with disease: mutations cause mitochondrial complex III deficiency (nuclear type 6), while reduced CYC1 expression links to decreased stroke risk in multi-omics analysis 4. CYC1 expression changes reflect altered metabolic states, including acute viral infection responses 5. These findings position CYC1 as both an essential respiratory component and a potential therapeutic target in cancer and metabolic diseases.