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. 2023 Mar 25;14(3):211. doi: 10.1038/s41419-023-05738-8

Fig. 5. Fatostatin decreases GPX4 protein synthesis through the AKT/mTORC1/4EBP1 axis.

Fig. 5

A RNA-seq and RT‒PCR results showed that the mRNA level of GPX4 was not significantly different between the DMSO and fatostatin groups. B, C Western blotting was used to analyze the GPX4 protein levels after the cells were treated with or without fatostatin (20 μM) for 24 h and CHX (50 μM) for different durations (0, 4, 8, 12 h). D Western blot analysis of the GPX4 protein levels in the U87 cells treated with DMSO, CQ (lysosomal inhibitor, 10 μM), or MG132 (proteasomal inhibitor, 10 μM) with or without fatostatin (20 μM) treatment for 24 h. Lower panels show the statistical analysis of the data, n = 3. E, F The protein expression levels of AKT, p-AKT, mTOR, p-mTOR, 4EBP1, and p-4EBP1 in U87 and U251 cells after fatostatin treatment for 24 h. G, H SC79 (AKT activator, 10 μM) reversed the relative protein expression levels of p-AKT, p-mTOR, p-4EBP1, and GPX4 in the U87 and U251 cells treated with fatostatin (20 μM) for 24 h. I, J MHY1485 (mTOR activator, 10 μM) reversed the changes in relative protein expression levels of p-mTOR, p-4EBP1, and GPX4 in the U87 and U251 cells treated with fatostatin (20 μM) for 24 h. *P < 0.05, **P < 0.01, ***P < 0.001; ns no significance.