Fig. 7: Mechanistic insights into iPLA2β–mediated suppression of lipid peroxidation and ferroptosis induced by p53 and ROS stress.

a Western blot analysis of U2OS ACSL4^−/−; GPX4^−/− cells transfected with AlOX12 or iPLA2β vector. The experiments were repeated twice, independently, with similar results. b Lipid peroxidation levels of U2OS ACSL4^−/−; GPX4^−/− cells transfected with ALOX12 or iPLA2β vector were treated with TBH (300 μM) and Ferr-1 (2 μM) as indicated for 8 h. c Quantification of lipid peroxidation levels as shown in (b). Error bars are mean ± s.d., n = 3 independent experiments. d Western blot analysis of U2OS ACSL4^−/−; GPX4^−/− cells transfected with iPLA2β or iPLA2γ vector. The experiments were repeated twice, independently, with similar results. e Quantification of Lipid peroxidation levels. U2OS ACSL4^−/−; GPX4^−/− cells with overexpression of iPLA2β or iPLA2γ were pre-incubated with Nutlin (10 μM) for 12 h, then treated with TBH (300 μM) and Nutlin (10 μM) as indicated for 8 h. f Quantification of cell death. U2OS ACSL4^−/−; GPX4^−/− cells with overexpression of iPLA2β or iPLA2γ were pre-incubated with Nutlin (10 μM) for 24 h, then treated with TBH (250 μM) and Nutlin (10 μM) as indicated. g Relative content of oxPE (18:0/22:4)sn2 in H1299 cells transfected with alox12, or/and iPLA2β (PE, phosphatidylethanolamines). p values were calculated using two-tailed unpaired Student’s t-test. Detailed statistical tests are described in the ‘Methods’. h Relative content of oxPE (18:0/20:4)sn2 in H1299 cells transfected ALOX12, or/and iPLA2β. i Quantification of cell death in H1299 cells transfected with vector, p53, iPLA2β WT or G517C, and additional TBH treatment. e–i Error bars are mean ± s.d., n = 3 biologically independent experiments. Source data are provided as a Source Data file.