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Fig. 2 | Molecular Medicine

Fig. 2

From: Targeting the NAT10/NPM1 axis abrogates PD-L1 expression and improves the response to immune checkpoint blockade therapy

Fig. 2

Acetylation-defective NPM1 fails to promote PD-L1 transcription and expression. A MDA-MB-231 cells were treated with trichostatin A (TSA, 5 μmol/L), nicotinamide (NAM, 5 mmol/L) or TSA and NAM for 12 h, and lysates were then subjected to immunoprecipitation with an anti-NPM1 antibody. B Schematic representation of the 7K-7R mutation in NPM1. C–E Vector, NPM1 wild-type overexpression plasmid (NPM1 WT) or NPM1 7K-7R mutant plasmid (NPM1 7 K-7R) was transfected into MDA-MB-231 cells. The promoter activity (C), mRNA level (D) and protein expression level (E) of PD-L1 were measured. F The Flag-NPM1 or Flag-NPM1 7K-7R mutant plasmid was transfected into MDA-MB-231 cells. A ChIP assay was performed with an anti-Flag antibody. Data are presented as the mean ± s.d. of three independent experiments. **P < 0.01; ***P < 0.001; ****P < 0.0001; ns, not significantly different

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