fig4

Cryptotanshinone differentially induces cell death in <i>ATP6V0D1</i>-deficient pancreatic cancer cells

Figure 4. Differential expression of FGFR2 partially determines cryptotanshinone sensitivity in ATP6V0D1-deficient cells. (A) CCK-8 assay showing cell viability after treatment with Crypto alone or in combination with various cell death inhibitors (Drug concentrations: Crypto, 5 μM; ZVAD-FMK, 50 μM; Ferr-1, 500 nM; VitE, 5 mM; NAC, 5 mM; Necro-1, 500 nM; Baf A1, 500 nM; treatment time: 12 h); (B) CCK-8 assay showing cell viability after treatment with Crypto alone or in combination with inhibitors (Drug concentrations: Crypto, 5 μM; ZVAD-FMK, 50 μM; Ferr-1, 500 nM; VitE, 5 mM; treatment time: 24 h); (C) Cell death assay showing the proportion of dead cells following treatment with Crypto alone or in combination with inhibitors (Drug concentrations: Crypto, 5 μM; ZVAD-FMK, 50 μM; Ferr-1, 500 Nm, VitE, 5 mM; treatment time: 24 h). Scale bar = 200 µm; (D and E) Western blot analysis showing protein expression in the indicated groups (Drug concentration: Crypto, 5 μM; treatment time: 24 h). Data (A-C) are shown as mean ± SD from at least three biologically independent samples (A and B, n = 6; C, n = 3). Statistical significance was analyzed using two-way ANOVA with Tukey’s multiple comparisons test. Western blots (D and E) represent three independent experiments. Source data are provided. *P < 0.05 was considered statistically significant; ns: not significant. FGFR2: Fibroblast growth factor receptor 2; ATP6V0D1: ATPase H+ transporting V0 subunit D1; SD: standard deviation; ANOVA: analysis of variance.

Cancer Drug Resistance
ISSN 2578-532X (Online)

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