Erol C. Bayraktar

TL;DR: In this article, a continuous-flow culture apparatus is used to maintain proliferating cancer cells in low-glucose conditions, demonstrating that mitochondrial oxidative phosphorylation (OXPHOS) is essential for optimal proliferation in these conditions; the most sensitive cell lines are defective in OXPHOS upregulation and may therefore be sensitive to current antidiabetic drugs that inhibit OPHOS.

TL;DR: A continuous-flow culture apparatus for maintaining proliferating cells in low-nutrient media for long periods of time is developed and used to undertake competitive proliferation assays, concluding that mtDNA mutations and impaired glucose utilization are potential biomarkers for identifying tumours with increased sensitivity to OXPHOS inhibitors.

TL;DR: It is found that loss of squalene monooxygenase expression alters the lipid metabolism of cancer cells, which confers protection from ferroptotic cell death and thus promotes tumour growth.

TL;DR: Iron homeostasis is identified as the key function of lysosomal acidity for cell proliferation, dramatically alters mitochondrial metabolism and hypoxia inducible factor (HIF) signaling due to iron depletion.

TL;DR: Findings provide a rationale for maintaining a compartmentalized one-carbon pathway in mitochondria, as SHMT2 null cells specifically fail to maintain formylmethionyl-tRNA pools and mitochondrially encoded proteins, phenotypes similar to those observed in MTFMT-deficient patients.