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• W3182982726 endingPage "102065" @default.
• W3182982726 startingPage "102065" @default.
• W3182982726 abstract "Although glucose, through pentose phosphate pathway (PPP), is the main source to generate NADPH, solid tumors are often deprived of glucose, hence alternative metabolic pathways to maintain NADPH homeostasis in cancer cells are required. Here, we report that lactate and glutamine support NADPH production via isocitrate dehydrogenase 1 (IDH1) and malic enzyme 1 (ME1), respectively, under glucose-deprived conditions. Isotopic tracing demonstrates that lactate participates in the formation of isocitrate. Malate derived from glutamine in mitochondria shuttles to cytosol to produce NADPH. In cells cultured in the absence of glucose, knockout of IDH1 and ME1 decreases NADPH/NADP+ and GSH/GSSG, increases ROS level and facilitates cell necrosis. In 4T1 murine breast tumors, knockout of ME1 retards tumor growth in vivo, with combined ME1/IDH1 knockout more strongly suppressing tumor growth. Our findings reveal two alternative NADPH-producing pathways that cancer cells use to resist glucose starvation, reflecting the metabolic plasticity and flexibility of cancer cells adapting to nutrition stress." @default.
• W3182982726 created "2021-07-19" @default.
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• W3182982726 date "2021-10-01" @default.
• W3182982726 modified "2023-10-18" @default.
• W3182982726 title "Lactate and glutamine support NADPH generation in cancer cells under glucose deprived conditions" @default.
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• W3182982726 doi "https://doi.org/10.1016/j.redox.2021.102065" @default.
• W3182982726 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8321918" @default.
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