Fig. 3. Blocking cystine uptake and resolving disulfide stress suppress high SLC7A11–induced cell death under H₂O₂ treatment.

a–c Measurement of intracellular concentrations of cystine (a), GSSG (b), and the GSSG/GSH ratio (c) in SLC7A11-low 786-O cells treated with vehicle or 1 mM H₂O₂ for 2 h and SLC7A11-high 786-O cells treated with vehicle or 1 mM H₂O₂ for 2 h with or without 5 μM erastin, 1 mM tris(2-carboxyethyl) phosphine (TCEP), 1 mM 2-mercaptoethanol (2-ME), 2 mM N-acetyl cysteine (NAC), 2 mM d-penicillamine (D-Pen), or 2 mM l- penicillamine (L-Pen). d, e Relative levels of intracellular γ-glutamyl-cystine (d) and γ-glutathionyl-cysteine (e) in SLC7A11-low 786-O cells treated with vehicle or 1 mM H₂O₂ for 2 h and SLC7A11-high 786-O cells treated with vehicle or 1 mM H₂O₂ for 2 h with or without 5 μM erastin, 1 mM TCEP, 1 mM 2-ME, 2 mM NAC, 2 mM d-penicillamine, or 2 mM l-penicillamine. f–k Cell death in response to 1 mM H₂O₂ treatment for 6 h with or without 5 μM erastin (f), 1 mM TCEP (g), 1 mM 2-ME (h), 2 mM NAC (i), 2 mM d-penicillamine (j), or 2 mM l-penicillamine (k) in SLC7A11-high 786-O cells measured using propidium iodide (PI) staining. l–q Cell death in response to 1 mM H₂O₂ treatment for 24 h with or without 5 μM erastin (l), 1 mM TCEP (m), 1 mM 2-ME (n), 2 mM NAC (o), 2 mM d-penicillamine (p), or 2 mM l-penicillamine (q) in T98G cells measured using PI staining. Data were presented as mean ± SD; n = 3. n indicates independent repeats. P value was determined by two-tailed unpaired Student’s t test. Source data are provided as a Source Data file.