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. 2019 May 10;24:101211. doi: 10.1016/j.redox.2019.101211

Fig. 2.

Fig. 2

Differential gene expression is trigged by ferroptosis. (A) FUF and FDF were identified by TMT, RNA-seq and DNase-seq in HepG2 cells. (B) Six FUF and 137 FDF were further identified by the TCGA database in liver cancer. (C) Ranking of FUF and FDF as fold changes in the normal liver compared to liver cancer, as analyzed by the TCGA database. (D) qPCR and Western blots of FUF and FDF in the control (treated with DMSO) and HepG2 or Bel-7402 cells treated with erastin (left: 10 μM, right: 5–20 μM) with or without ferrostatin-1 (1 μM) for 24 h. (E) Representative IHC images of HBA1 and STMN1 in DEN/CCl4-induced mouse liver cancer or xenografts formed by Bel-7402 cells. Mice were treated with DMSO or erastin (for DEN/CCl4 mice: 10 mg/kg; for xenograft mice: 5 mg/kg) with or without ferrostatin-1 (for DEN/CCl4 mice: 2 mg/kg; for xenograft mice: 1 mg/kg) after liver cancer and xenografts were formed. Scale bar, 200 μm n = 5/group. (F) Expression of HBA1 and STMN1 in human liver cancer and paired normal liver tissues, as measured by Western blotting and IHC. Scale bar, 200 μm. The data are shown as the means + SD from three independent experiments (Fig. 2d). Images of IHC and WB are representative ones of 3–5 independent experiments. **, p < 0.01 indicate statistical significance. The data from Fig. 2d were analyzed by a one-way ANOVA test.