Bile acids inhibit ferroptosis sensitivity through activating farnesoid X receptor in gastric cancer cells

Figure 5 Farnesoid X receptor exerted anti-ferroptosis effects by inhibiting BTB and CNC homology 1. A and B: Protein expression of BTB and CNC homology 1 (BACH1) in gastric cancer (GC) cells transfected with the shNC or shFXR plasmid for 24 h; C and D: Western blot (WB) analysis of BACH1 protein expression in GC cells transfected with the shNC or shFXR plasmid for 24 h; E and F: HGC-27 and MKN-45 cells were transfected with the control or BACH1-coding plasmid and confirmed through WB analysis; G-I: Malondialdehyde production and BODIPY-589/591 C11 staining of GC cells after transfection with the farnesoid X receptor (FXR)-coding plasmid together with or without the BACH1-coding plasmid and erastin treatment (5 μM) for 24 h; J-M: Alterations of glutathione (GSH) concentrations and the GSH/oxidized GSH ratio in HGC-27 and MKN-45 cells after transfection with the FXR-coding plasmid together with or without the BACH1-coding plasmid; N and O: WB analysis of GCLC, GSS, GCLM, and GSH peroxidase 4 protein expression after transfection with the FXR-coding plasmid together with or without the BACH1-coding plasmid. Scale bar: 100 μm. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. These experiments were repeated three times. FXR: Farnesoid X receptor; BACH1: BTB and CNC homology 1; GSH: Glutathione; GSSG: Oxidized glutathione; GPX4: Glutathione peroxidase 4.