Fig. 4: OSGIN1 inhibited SLC2A3 through the AMPK/mTOR pathway.
From: A targetable OSGIN1 − AMPK − SLC2A3 axis controls the vulnerability of ovarian cancer to ferroptosis

a A Venn diagram of the FerrDb database established by crossing related genes in the DEG and FerrDb datasets. b Volcano maps for the 21 genes. c SLC2A3 mRNA expression in SKOV3 and OVCAR3 cells with OSGIN1 knockdown or OSGIN1 overexpression. N = 3 samples. d, e The protein expression levels of t-AMPK, P-AMPK, t-mTOR, P-mTOR, and SLC2A3 were determined by Western blotting. f Dot plot of the KEGG pathway enrichment analysis. The horizontal axis represents the gene ratio, while the vertical axis represents the enriched pathway. The color scale indicates different thresholds of the p value, and the size of the dot indicates the number of genes corresponding to each pathway. g The expression of t-mTOR, P-mTOR, and SLC2A3 in ovarian cancer cells treated with 1 mmol/L AICAR (activator of AMPK) or 50 μmol/L compound C (inhibitor of AMPK) for 24 h. h Rapamycin stimulates SLC2A3 promoter activity. Activity of SLC2A3 promoter-driven luciferase reporter was measured in SKOV3 (Left) and OVCAR3 (Right) cells treated with or without 100 nM rapamycin for 24 h. Each experiment was repeated three times. The p values in c and g were determined by two-way ANOVA with multiple comparisons. The p values in e and h were determined by one-way ANOVA with multiple comparisons. Error bars are s.e.m. **p < 0.01; ***p < 0.001.