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. 2023 Jun 19;13(6):e1300. doi: 10.1002/ctm2.1300

FIGURE 4.

FIGURE 4

SLC7A11 mediates the regulatory effect of DUXAP8 on ferroptosis. (A, B) The DUXAP8 knockdown‐induced increases of intracellular MDA concentration and GSSG/GSH ratio level were reversed by SLC7A11 overexpression in both LM3 and HepaRG cells untreated and treated with erastin and sorafenib. (C) Representative IF images showed that the cellular lipid ROS (green) and Fe2+ (orange) levels were elevated by sh‐DUXAP8 transfection and the elevation could be reversed by SLC7A11 overexpression in LM3 cells untreated and treated with erastin and sorafenib. Magnification: ×400. (D, E) The DUXAP8 knockdown‐induced increases of intracellular MDA concentration and GSSG/GSH ratio level were reversed by SLC7A11 overexpression in both Huh7 and PLC cells untreated and treated with erastin and sorafenib. (F) Representative IF images showed that the cellular lipid ROS (green) and Fe2+ (orange) levels were elevated by sh‐DUXAP8 transfection and the elevations could be reversed by SLC7A11 overexpression in Huh7 cells untreated and treated with erastin and sorafenib. Magnification: ×400. * p < 0.05, ** p < 0.01, *** p < 0.001. NS, not significant. Results represent three independent experiments. sh‐DUX, sh‐DUXAP8; EV, Empty vector; OE, pcDNA DUXAP8; sh‐SLC, sh‐SLC7A11; OE‐SLC: pcDNA SLC7A11.