Fig. 7
Integrative transcriptomic and epigenomic analyses of SPI1 function in HNSCC. a Heatmaps and averaged ChIP-seq signal profiles showing SPI1 occupancy around transcription start sites (TSSs) in SPI1-overexpressing SAS cells, with SPI1 ChIP-seq Rep1 and its corresponding input control shown separately. b Aggregated metagene profiles illustrating normalized SPI1 ChIP-seq read density relative to the TSS across two independent SPI1-OE ChIP replicates and matched input samples. c Circos plot showing the genome-wide chromosomal distribution of SPI1 ChIP-seq binding peaks. d Volcano plot of DEGs identified by RNA-seq following SPI1 overexpression. DEGs were defined using an FDR < 0.05 and a |log2FC| > 1. e Representative gene set enrichment analysis (GSEA) plots showing hallmark pathways enriched in SPI1-overexpressing cells. f Venn diagram depicting the overlap between genes upregulated upon SPI1 overexpression and genes annotated with SPI1 ChIP-seq binding peaks. g Bubble plot showing Gene Ontology (GO) biological process enrichment of genes coregulated by SPI1 transcriptional activation and direct chromatin binding; the dot size indicates the gene count, and the color represents the adjusted P value. h De novo motif analysis of SPI1 ChIP-seq binding peaks. i Dual-luciferase reporter assay measuring SPI1-dependent transcriptional activity in a doxycycline-inducible system over time (n = 3 independent experiments; mean ± SD; one-way ANOVA with Tukey’s post hoc test)
