Fig. 2: NINJ1 knockdown-mediated ferroptosis protection is abolished by the inhibition of CoA and GSH synthesis.
From: NINJ1 regulates ferroptosis via xCT antiporter interaction and CoA modulation
A The heatmap showed the relative cell viability (% of DMSO- or compound-treated cells under erastin treatment) of control and NINJ1-knockdown HT-1080 cells, as summarized from the cell viability graphs in Fig. 2B–D and supplemental Fig. 2. Each cell viability graph was generated individually using the CellTiter-Glo assay following treatment with the indicated concentrations of erastin, with or without the specified compounds. The relative viability percentages for cells treated with 5 μM erastin, combined with or without the indicated compounds, were then compiled into the heatmap. B–D Cell viability of control and NINJ1-knockdown HT-1080 cells were determined by CellTiter-Glo assay following treatment with erastin (5 μM) and ferrostatin-1 (Fer-1, 10 μM), with or without either (B) pantothenate kinase inhibitor (PANKi, 5 μM), (C) buthionine sulfoximine (BSO, 500 μM), or (D) diethylmaleate (DEM, 200 μM) for 24 h. E Intracellular CoA levels of control and NINJ1-knockdown HT-1080 cells following erastin treatment (1.25 μM, 24 h) were determined by Coenzyme A Assay Kit. F The GSH/GSSG ratio of control and NINJ1-knockdown HT-1080 cells following erastin treatment (1.25 μM, 24 h) were measured by the GSH/GSSG-Glo Assay. Error bars in (B–F) represent SEM (n = 3+).
