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

Figure 3 Bile acids inhibited ferroptosis sensitivity of gastric cancer cells by activating farnesoid X receptor. A and B: Cell viability of erastin-treated HGC-27 and MKN-45 cells with or without GW4064 treatment; C and D: HGC-27 and MKN-45 cells were transfected with shFXR or shNC plasmid. Successful construction was confirmed by western blot analysis; E and F: Cell viability assay of GC cells treated with different concentrations of erastin and CDCA (50 μM) transfected with shFXR or shNC for 24 h; G-I: Malondialdehyde (MDA) production and BODIPY-589/591 C11 staining of GC cells transfected with shFXR or shNC plasmid and treated with erastin together with or without CDCA for 24 h; J and K: GC cells were transfected with control or FXR-coding plasmid and confirmed through western blot analysis; L and M: Cell viability assay of GC cells treated with different concentrations of erastin and CDCA (50 μM) transfected with control or FXR-coding plasmid for 24 h.; N-P: MDA production and BODIPY-589/591 C11 staining of GC cells transfected with control or FXR-coding plasmid and treated with erastin together with or without CDCA for 24 h. Scale bar: 100 μm. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001. These experiments were repeated three times. FXR: Farnesoid X receptor; NC: Negative control; CDCA: Chenodeoxycholic acid; MDA: Malondialdehyde; NS: Not significant.