fig2

Corosolic acid increases the therapeutic effect of cisplatin on gastric cancer by regulating Gpx4-dependent ferroptosis

Figure 2. The effect of CA as a chemosensitizer in GC cells was damaged by Fer-1. AGS (A) and AGS-CR (B) cells were exposed to cisplatin (35 µm) and CA (5 µm) or Ferrostatin-1 (Fer-1, 1 μm) for 24 h, and then cell viability was measured using the CCK-8 assay (n = 3). Statistical significance was assessed using one-way ANOVA followed by Tukey’s post-hoc test. AGS-CR cells were exposed to cisplatin (35 µm) and CA (5 µm) in the presence or absence of Fer-1 (1 μm), and then clone formation assay (C) and quantitative analysis (D) were carried out (n = 3). Statistical significance was assessed using Student’s t test. AGS-CR cells were exposed to cisplatin (35 µm) and CA (5 µm) in the presence or absence of Fer-1 (1 μm), and then FDA staining (E) and quantitative analysis (F) were performed (n = 3). Statistical significance was assessed using Student’s t test. *P < 0.05, **P < 0.01, ***P < 0.001. CA: Corosolic acid; GC: gastric cancer; CR: cisplatin-resistant; CCK-8: cell counting kit-8; FDA: fluorescein diacetate.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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