Fig. 4: EWS/FLI-driven transcriptional regulation diminished by FLI DBD flanking deletions in Ewing sarcoma cells. | Oncogene

Fig. 4: EWS/FLI-driven transcriptional regulation diminished by FLI DBD flanking deletions in Ewing sarcoma cells.

From: The FLI portion of EWS/FLI contributes a transcriptional regulatory function that is distinct and separable from its DNA-binding function in Ewing sarcoma

Fig. 4

A–B Venn diagram analysis of RNA-sequencing data comparing genes significantly A activated or B repressed in A673 cells rescued with the indicated constructs (full-length EWS/FLI [EF], EF DBD, and EF DBD+) when compared to A673 cells with no exogenous EWS/FLI construct (iEF + Empty Vector) (adjusted p-value (FDR) < 0.05; N = 3 biological replicates each). C–D GSEA analysis comparing all genes regulated by EF DBD+ as the rank-ordered gene list to a gene set of C genes activated by EF DBD (log2(FC) > 1.5, FDR < 0.05) or D genes repressed by EF DBD (log2(FC) < −1.5, FDR < 0.05) as the gene set. E Genes significantly activated by endogenous EWS/FLI were defined using a previous RNA-sequencing dataset [32]. Genes activated by EF, EF DBD, and EF DBD+ in A673 knock-down/rescue cells were compared to this list of EWS/FLI-activated genes. Scatterplots comparing genes activated by EF (on the x-axis) to EF DBD+ (left) or EF DBD (right) (on the y-axis) were plotted to determine the ability of these constructs to rescue expression these genes. Significance was defined by a log2(FC) > 0 and an adjusted p-value < 0.05. Pearson correlation coefficient and associated p-values with slope are noted on the plots. Pie charts represent the proportion of genes found in each of the described groups.

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