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. 2024 Mar 11;12(3):e008554. doi: 10.1136/jitc-2023-008554

Figure 5.

Figure 5

Knockdown of LPCAT3 suppressed mefloquine+IFN-γ-induced ferroptosis. (A) The relative mRNA expression of LPCAT3 in B16F10 and LLC cells expressing sh-Mock or two independent sh-LPCAT3 was determined (n=3 replicate cultures for each cell type). (B) Immunoblots of LPCAT3 in B16F10 and LLC cells expressing sh-Mock or two independent sh-LPCAT3 are shown. (C) The ROS levels in B16F10 and LLC cells expressing sh-Mock or two independent sh-LPCAT3 constructs treated with Mef (4 µM) or IFN-γ (20 ng/mL) were determined (n=3 replicate cultures for each cell type). (D) The lipid peroxidation levels in B16F10 and LLC cells expressing Mock or two independent shLPCAT3 constructs treated with Mef (4 µM) or IFN-γ (20 ng/mL) were determined (n=3 replicate cultures for each cell type). (E) The numbers of B16F10 and LLC cells expressing Mock or two independent shLPCAT3 constructs treated with Mef (4 µM) or IFN-γ (20 ng/mL) (n=6 replicate cultures for each cell type) were determined. All the data are presented as the mean (±SD). One-way analysis of variance was performed for comparisons among multiple groups. Statistical significance was assessed according to statistical methods (*p<0.05; **p<0.01; and ***p<0.001). IFN, interferon; LLC, Lewis lung cancer; LPCAT3, lysophosphatidylcholine acyltransferase 3; Mef, mefloquine; mRNA, messenger RNA; ROS, Reactive oxygen species.