Fig. 3: Inhibiting LDHB and the SLC7A11/GSH/GPX4 axis confers ferroptosis-mediated metabolic synthetic lethality.
From: Lactate dehydrogenase B noncanonically promotes ferroptosis defense in KRAS-driven lung cancer

a Immunoblot of the indicated cells stably transduced with shNT or shRNAs against LDHB. b Clonogenic assay of murine KP cells transduced with shLdhb#b and shNT and further treated for 72 h with erastin (15 μM) or DMSO. c Quantitative analysis (qPCR) of PTGS2 mRNA in the indicated cells treated for 14 h with DMSO or erastin (A549, 5 µM; H838, 2.5 µM) with or without FER1 (3 µM). d–f Viability assay of shNT- or shLDHB-transduced cells after treated with RSL3 or erastin, alone or in combination with 2 μM Ferrostatin-1(FER1). g Flow cytometry of C11 BODIPY mean fluorescence intensity ratio of oxidative channel (FITC 488 nm) versus non-oxidative channel (PE-TEXAS RED 610 nm) in shNT- or shLDHB-transduced cells. A549 cells were treated with 0.5 μM RSL3 or 5 μM erastin, alone or in combination with 2 μM FER1 for 6 h and 14 h, respectively. H838 cells were treated with 0.25 μM RSL3 or 2.5 μM erastin, alone or in combination with 2 μM FER1 for 6 h and 14 h, respectively. Data are shown as mean ± s.d (n = 3), with statistical analyses by two-way ANOVA. h Colony assay of A549 and H838 shNT- or shLDHB-transduced cells treated with erastin (A549, 5 µM; H838, 2.5 µM) or sulfasalazine (SSZ; A549, 0.25 mM; H838, 1 mM) for 24 h in the presence or absence of NAC (10 mM).