Nature: Mitochondria ubiquitin oxidation is a necessary condition for tumor growth

Mitochondrial electron transfer chain (ETC) is essential for tumor growth, combined with targeted therapy, etc inhibition has been shown to have anti-tumor effectIn addition, the human brain and lung tumor mitochondria have a strong glucose oxidation capacityHowever, until now, it is still unclear why a functional ETC is necessary for tumor growth in the bodyTHE FUNCTIONS OF ETC ARE INTEGRATED TO PRODUCE ATP, I.EOXIDATION PHOSPHORYLATION AND THE PRODUCTION OF METABOLITES BY THE TRIAINIC ACID (TCA) CYCLEMitochondrial complexes I and II are electronically donated to ubiquinox, resulting in the generation of panmylycol and the regeneration of NAD plus and FAD cofactors, the compound III oxidizes ubiquinol sourcin back to ubiquinone, and ubiquity can also be used as an electronic receptor of dihydrotide dehydrogenase (DHODH) -- an enzyme necessary for the synthesis of a new glycosinerecently, researchers found that tumor growth in the absence of mitochondrial complex III was impairedThis phenotype was saved by the ectopicly expressed Ciona intestinal alternative oxidase (AOX), which also oxidizes ubiquinol into ubiquinoxThe loss of mitochondrial complexI, II, or DHODH reduces tumor growth that lacks mitochondrial complex III but expresses AOX, highlighting the need for pantominotometry as an electronic receiver for tumor growthtumor cells lacking mitochondrial complex III can regenerate NAD-plus by expressing LACTis (LbNOX) NADH oxidase, but they are still unable to growsuggests that the regeneration of NAD plus is not enough to drive the growth of tumors in the bodyin general, the results show that tumor growth requires ETC to oxidize ubiquinone, which is essential for driving oxidation TCA cycle and DHODH activity