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(1) Elegant work demonstrating a casual role for mitochondrial metabolism in tumorigenesis. Congrats to the authors! A few thoughts below 
Oxidative Metabolism Drives Immortalization of Neural Stem Cells during Tumorigenesis https://www.cell.com/cell/fulltext/S0092-8674(20)30947-8#.X1pvPlbX2I9.twitter
Oxidative Metabolism Drives Immortalization of Neural Stem Cells during Tumorigenesis https://www.cell.com/cell/fulltext/S0092-8674(20)30947-8#.X1pvPlbX2I9.twitter
(2) Throughout the paper, the authors repeatedly link various measurements of mitochondrial function (e.g., respiration, TCA cycle flux, gene expression) to OXPHOS. The term âOXPHOSâ refers to a specific function where the proton motive force is used to phosphorylate ADP.
(3) Unlike in glycolysis, where ADP phosphorylation is integral to enzyme catalysis, ATP synthesis in the mitochondria is just one, of many, processes fueled by âoxidative fluxâ. In other words, OXPHOS does not equal respiration. In the present paper, OXPHOS was not measured.
(4) Rather, O2 consumption, TCA cycle flux and gene expression were. There seems to be a trend to link such measurements to OXPHOS in cancer. It may seem trivial, but I think it is important to make the distinction that such measurements are NOT OXPHOS readouts.
(5) Lumping all measurements of mitochondrial function as OXPHOS readouts oversimplifies mitochondrial bioenergetics and discounts the nuance that is mitochondrial OXPHOS! Critical mechanistic insight often lurks in the nuance.
(6) e.g., Fig 7 experiments with yeast ND1 suggest that âATP synthesisâ per se is not what is required for tumorigenesis, reminiscent of recent findings from the Chandel Lab @inma_mreyes https://www.nature.com/articles/s41586-020-2475-6. Not being critical, just embracing the nuance. #mitochondria
