KEAP1 deficiency drives glucose dependency and sensitizes lung cancer cells and tumors to GLUT inhibition

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H2A monoubiquitination links glucose availability to epigenetic regulation of the endoplasmic reticulum stress response and cancer cell death

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High cell density increases glioblastoma cell viability under glucose deprivation via degradation of the cystine/glutamate transporter xCT (SLC7A11)

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LKB1 and KEAP1/NRF2 pathways cooperatively promote metabolic reprogramming with enhanced glutamine dependence in KRAS-mutant lung adenocarcinoma

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The Non-Essential Amino Acid Cysteine Becomes Essential for Tumor Proliferation and Survival

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BAP1 links metabolic regulation of ferroptosis to tumour suppression

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Cystine uptake through the cystine/glutamate antiporter xCT triggers glioblastoma cell death under glucose deprivation

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Keap1 loss promotes Kras-driven lung cancer and results in dependence on glutaminolysis

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CDK20 interacts with KEAP1 to activate NRF2 and promotes radiochemoresistance in lung cancer cells

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BAP1 inhibits the ER stress gene regulatory network and modulates metabolic stress response

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The glutamate/cystine xCT antiporter antagonizes glutamine metabolism and reduces nutrient flexibility

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Environmental cystine drives glutamine anaplerosis and sensitizes cancer cells to glutaminase inhibition

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LncRNA NBR2 engages a metabolic checkpoint by regulating AMPK under energy stress

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Role of KEAP1 / NRF2 and TP53 Mutations in Lung Squamous Cell Carcinoma Development and Radiation Resistance

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FoxO Transcription Factors Promote AKT Ser473 Phosphorylation and Renal Tumor Growth in Response to Pharmacologic Inhibition of the PI3K–AKT Pathway

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