Fig. 7: ETS2 is the key gene through which NAT10 indirectly regulates PD-L1 via ac4C acetylation. | Cell Death & Disease

Fig. 7: ETS2 is the key gene through which NAT10 indirectly regulates PD-L1 via ac4C acetylation.

From: Targeting the ac4C ‘Writer’ NAT10 enhances pancreatic cancer immunotherapy via dual modulation of CD8+ T cells and tumor cells

Fig. 7: ETS2 is the key gene through which NAT10 indirectly regulates PD-L1 via ac4C acetylation.

A The UMAP plot illustrates the distribution of KRT8 across different cells in the single-cell data. B The cell-cell communication plot illustrates the interactions between epithelial cells with high and low expression of KRT8 and different cells. C Correlation analysis (GEPIA) revealedassociations between KRT8 and CD274 (P = 0.96, R = 0.0042). D The hierarchical plot illustrates the interactions between epithelial cells with high and low expression of KRT8 and different cells. E Workflows of RNA-seq, acRIP-seq, and ATAC-seq showing the identification of target transcription factors (TFs) regulated by NAT10. F Volcano plot showing chromatin accessibility changes in NAT10-knockdown cells (ATAC-seq analysis). G Conjoint analysis identified key transcription factors, including ETS2, through RNA-seq, acRIP-seq, and ATAC-seq integration. H Venn diagram showing the overlap of differentially expressed transcription factors and acetylated transcripts, highlighting ETS2 as a central target. I GEPIA revealed significantly elevated ETS2 expression in pancreatic cancer tissues compared with normal tissues. J acRIP-seq peak visualization of ETS2 mRNA showing ac4C enrichment in control cells. K Correlation analysis (GEPIA) revealed positive associations between ETS2 and NAT10 (P = 0.0023, R = 0.22) as well as between ETS2 and PD-L1 (P = 0.0034, R = 0.22).

Back to article page