Fig. 9: Genes highly upregulated in Ascl1-OE tumors are important for NSC maintenance, cancer metastasis and invasion, and therapeutic resistance. | Nature Communications

Fig. 9: Genes highly upregulated in Ascl1-OE tumors are important for NSC maintenance, cancer metastasis and invasion, and therapeutic resistance.

From: Transcription factors ASCL1 and OLIG2 drive glioblastoma initiation and co-regulate tumor cell types and migration

Fig. 9: Genes highly upregulated in Ascl1-OE tumors are important for NSC maintenance, cancer metastasis and invasion, and therapeutic resistance.

a Differentially expressed genes (DEGs) significantly up- or downregulated by comparing cell type x cell type between control and Ascl1-OE tumors. DEGs include both ASCL1 target and non-target genes. b Gene ontology analysis of upregulated DEGs showing enrichment of genes important for protein synthesis and mitochondrial function. c, d Heatmap of Unionized Cell-Type RNA-seq (columns) demonstrating upregulation of ribosomal (c) and mitochondrial (d) genes (rows) in Ascl1-OE tumors. e UMAPs showing specific upregulation of cytochrome C oxidase subunit genes. f, g Top 25 genes upregulated (f) or downregulated (g) in ≥ 5 cell types, with delineation of ASCL1 targets and known functions in cancer or GBMs. Bar graphs are mean Log2 Fold Change ± SEM for indicated genes by comparing cell type x cell type between control and Ascl1-OE tumors. Open circles within each bar graph represent number of cell types with indicated genes significantly altered (adjusted p-value < 0.05). UMAP gene expression of 3 of the topmost upregulated (h) and downregulated (i) genes. Proportions of tumor cells expressing these genes are indicated for control and Ascl1-OE tumors.

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