Fig. 5: Diverse oncogenic mechanisms induced by ecNR2E1.
a Reconstruction of ecNR2E1 circular amplification based on scATAC data. b Kaplan–Meier analysis of overall survival in TCGA-GBM patients separated by NR2E1 expression. c Volcano plot showing differentially expressed genes from ecNR2E1 patient-derived malignant cells compared to malignant cells from other patients, with fold change (FC) and adjusted P value (adj.P) calculated using the FindAllMarkers function. Genes with Log2FC > 0.5 and adj.P < 0.05 were considered upregulated. Differentially expressed TFs and oncogenes in the constructed ecNR2E1 network were highlighted in blue, while differentially expressed genes carried by ecNR2E1 were marked in red. d Violin plots showing the expression of CD24, NR2E1, and FOXO3 in malignant cells from ecNR2E1 and other patients. Statistical significance was assessed using a two-sided Wilcoxon test. e Meta-cells of ecNR2E1 and other patient-derived malignant cells were constructed, and the correlation between CD24 and NR2E1 counts was calculated using the Pearson method. Boxplots showing CD24 and NR2E1 counts for each group. Statistical significance was assessed using a two-sided Wilcoxon test. ns, no significance; *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001. f TF regulatory network depicting the candidate target genes for NR2E1 and FOXO3 in malignant cells from the ecNR2E1 patient. The network included 511 of the 1045 upregulated genes identified in ecNR2E1 patient-derived malignant cells. g Enhancer activity analysis identified candidate enhancers that correlated with FOXO3 expression, contained NR2E1 recognition motifs and were differentially active between malignant cells from ecNR2E1 and non-ecNR2E1 patients.
