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. 2022 May;11(5):786–801. doi: 10.21037/tlcr-22-318

Figure 6.

Figure 6

By targeting GPX4, RSL3 induced EGFR-TKI-resistant LUAD cell death via ferroptosis. RSL3 exerted stronger dose-dependent killing effects on EGFR-TKI resistant cells than Erastin. (A) Proliferation inhibition curves of HCC827GR/HCC827 and PC9OR/PC-9 cells after treatment with RSL3. (B) Proliferation inhibition curves of HCC827GR/HCC827 and PC9OR/PC-9 cells after treatment with Erastin. (C) PI staining analysis of HCC827GR and PC9OR cells after exposure to RSL3 (1 µM) for 0, 8, and 16 h. (D) Representative phase-contrast microscopy images of HCC827GR and PC9OR cells after treatment with 1 and 5 µM RSL3 for 16 h, respectively (magnification, ×100). (E) HCC827GR and PC9OR cells were treated with 1 µM RSL3 for 0, 8 and 16 h, respectively, and then with DCFH-DA for 20 min to detect the ROS level by flow cytometry. (F) Immunofluorescence revealed the aggregation of ROS in HCC827GR and PC9OR cells (magnification, ×100). Data are exhibited as the mean ± standard error based on at least three independent experiments. Significant differences were defined by one-way Analysis of Variance (ANOVA) with a Bonferroni post-hoc test. ***, P<0.001. ROS, reactive oxygen species; DCFDA, 6-carboxy-2',7'-dichlorofluorescein diacetate dye; EGFR, epidermal growth factor receptor; TKI, tyrosine kinase inhibitor; LUAD, lung adenocarcinoma.