Hypoxia Enhances Glioma Resistance to Sulfasalazine-Induced Ferroptosis by Upregulating SLC7A11 via PI3K/AKT/HIF-1α Axis

Figure 3

Hypoxia promoted SAS resistance via increasing SLC7A11 expression. (a) SLC7A11 protein expression level. SLC7A11 knockdown can significantly inhibit the protein expression level. (b) The growth curves were examined using a CCK-8 assay. SLC7A11 knockdown did not influence the cell proliferation rate of glioma cells. (c) Cell viability curves at different concentrations of SAS for 24 h. SLC7A11 knockdown could reverse the enhanced SAS resistance induced by hypoxia. (d) The IC₅₀ of SAS in SLC7A11 knockdown group was obviously low than that of scramble group under hypoxic or normoxic condition. (e) Clone formation assay of cancer cells in the absence or presence of SAS for 2 weeks. SLC7A11 knockdown could reverse the enhanced cell colony formation ability induced by hypoxia. The bar graph showed of 3 independent experiments. and .

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