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Importantly, several studies have showed that inhibiting SLC7A11 activities suppresses glutamine-derived glutamate export, enhance glutamate to replenish the TCA cycle intermediates, and promote ROS production [63, 71, 72], suggesting that SLC7A11 antagonizes pro-ferroptotic glutaminolysis and that increasing glutamine metabolism under blockage of GSH synthesis upregulates ROS levels and promotes ferroptosis, which may provide a novel treatment guideline option for ferroptosis-based tumor therapy

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PubMed CrossRef Anton RF, Myrick H, Wright T.M, et al

[DOI] [PubMed] [Google Scholar] 38.Atli T, Keven K, Avci A, et al
