Fig. 1: NINJ1 knockdown protected against ferroptosis specifically triggered by class I FINs.
From: NINJ1 regulates ferroptosis via xCT antiporter interaction and CoA modulation
A–E Cell viability of HT-1080 cells, transduced with a control vector or two NINJ1-targeting shRNA, was determined by CellTiter-Glo assay following treatment with indicated concentrations of (A) erastin (23 h), (B) sulfasalazine (28 h), (C) RSL3 (19 h), (D) FIN56 (19 h), and (E) FINO2 (19 h). F-G NINJ1 knockdown abolished erastin-induced membrane rupture in HT-1080 cells. Membrane rupture of control and NINJ1-knockdown HT-1080 cells were observed by CellTox Green under fluorescence microscopy (F) and quantified (G) following erastin treatment (2.5 and 5 μM, 22 h). Scale bar: 400 μm. H-I NINJ1 knockdown inhibited erastin-induced lipid peroxidation in HT-1080 cells. Lipid peroxidation of control and NINJ1-knockdown HT-1080 cells were determined by C11-BODIPY staining (H) and quantified by % of lipid peroxidation positive cells (I) following erastin treatment (2.5 μM, 20 h). J-K Cell viability of HT-1080 cells was determined by CellTiter-Glo assay following treatment with indicated concentrations of (J) erastin (24 h) or (K) sulfasalazine (48 h) combined with glycine (5 or 10 mM). Error bars in (A–E), (G), (I), and (J-K) represent SEM (n = 3+).
