Fig. 5: PPP1R15A promotes MYC silencing and G2M phase arrest.

A GO functional enrichment bubble diagram of differentially expressed phosphorylated peptides in PPP1R15A vs. Vector group under biological process classification. B Comparation of mRNA transcription expression level (FPKM) in PC-3 transfected with vector and PPP1R15A. C Gene lengths of up and downregulated by PPP1R15A (Log2FC ≥ 1 and P ≤ 0.05). D GSEA analysis of transcriptome sequencing data of vector and PPP1R15A based on Hallmark genes sets. E, F The genes in the PPP1R15A group were negatively enriched to the MYC targets. G Relative mRNA expression level of MYC was assessed by RT-qPCR. H The genes in the PPP1R15A group were negatively enriched to the G2M checkpoint. I Flow cytometry assay revealed cell cycle in PC-3 under indicated condition. ES, elesclomol. J Quantitation of Fig. 5I. K Quantitation of cell cycle in BT-549 under indicated condition. L PPI network between MYC and core enrichment genes of G2M checkpoint in GSEA. M Relative mRNA expression level of MYC and its targets was assessed by RT-qPCR. N Forced expression of MYC alleviated G2M phase arrest in PPP1R15A overexpression PC-3. For elesclomol treatment, media were supplemented with 1 μM CuCl2. Data are presented as the means ± SD from independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.