Fig. 5: Mechanism of p53-related antitumor activity of FP NPs in vitro.
a Western blotting analysis of p53 in cells after treatment with 4 μM of different formulations (dosage based on Fluplatin) for 12 h. Their grayscale values were quantified (b–e) (n = 3 independent samples; one-way ANOVA followed by Tukey’s HSD post hoc test). f Western blotting analysis of p53 in cells after treatment with different concentrations of FP NPs for 12 h. Their grayscale values were quantified (g, h) (n = 3 independent samples; one-way ANOVA followed by Tukey’s HSD post hoc test). i Western blotting analysis of p53 in cells after treatment with 4 μM of FP NPs for 12 h. And their grayscale values were quantified (j) (n = 3 independent samples; one-way ANOVA followed by Tukey’s HSD post hoc test). k Western blot of cells treated with 4 μM FP NPs or not for 12 h and cultured in medium containing 10 μM MG132 or 10 mM 3-MA. Their grayscale values were quantified (l) (n = 3 independent samples; one-way ANOVA followed by Tukey’s HSD post hoc test). Western blot of H1975 (m), H2087 (n), H2342 (o), and A549 (p) cells treated with 2 μM FP NPs or not for 12 h and then treated with 100 μg/mL CHX at the indicated time points. n = 3 biologically independent samples, relative p53/actin ratios are shown. q Western blotting analysis of total ubiquitination (Ub) of immunoprecipitated (IP) p53 in cells after treatment with 2 μM FP NPs with or without MG132 (n = 3 independent samples). r HMGR inhibition assay under different formulations (n = 3 independent samples; one-way ANOVA followed by Tukey’s HSD post hoc test). s The volcano plot shows differential expression of FP NPs treated and untreated H1975 cells. t Schematic summary of the p53-related antitumor mechanism of FP NPs. Data are shown as the mean ± SD; n.s. no significance. Source data are provided as a Source Data file.
