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. 2026 Jan 1;16(6):2952–2983. doi: 10.7150/thno.124189

Figure 5.

Figure 5

MCT-NE#9 induces breast cancer ferroptosis. Confocal laser scanning microscopy images of (A) LPO, (B) iron ion accumulation, and (C) ROS generation after treatment with blank-NE, MTD, MCT and MCT-NE#9. Scale bar: 20 μm. Flow cytometry of ferroptosis after treatment with blank-NE#9, MTD, MCT, and MCT-NE#9. (D) Quantification of the MFI of LPO. (E) Quantification of the MFI of iron ion accumulation. (F) Quantification of the MFI of ROS. Values are shown as mean ± SEM (n = 3 per group). (G) Quantification of the percentages of CD71 after treatment with MTD, MCT, and MCT-NE#9. Values are shown as mean ± SEM (n = 3 per group). (H) Histogram representation of CD71 expression levels, corresponding to the quantification shown in panel (G). (I) Quantification of HMGB1 levels measured by ELISA after treatment with MTD, MCT, and MCT-NE#9. Values are shown as mean ± SEM (n = 4 per group). (J) Representative western blot analysis of SLC7A11 and GPX4 protein expression in the control, MTD, MCT, and MCT-NE#9 groups. β-actin was used as a loading control. (K) Quantification of GPX4 protein expression (fold change) normalized to β-actin, corresponding to the western blot results in panel (J). Values are shown as mean ± SEM (n = 3 per group). (L) Quantification of SLC7A11 protein expression (fold change) normalized to β-actin, corresponding to the western blot results in panel (J). Values are shown as mean ± SEM (n = 3 per group). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.