Fig. 5: Endocan induces changes in the chromatin structure in the Myc promoter region.

a ATAC-seq analysis of tumors derived from Esm1 WT and KO mice (n = 2 mice per group). Individual dots represent peaks located in gene promoter region (red), in transcribed sequence (blue) and outside of the gene (gray). b Volcano plot showing differentially expressed genes (LogFC expression (p < 0.05) between tumors derived from Esm1 WT and KO mice as determined by RNAseq analysis. (n = 3 mice per group). Genes with altered chromatin structure of their promoter region as determined by ATAC-seq analysis are indicated with red dots. c Sequencing read coverage of Myc gene as determined by RNA-seq (gene expression; blue) and ATAC-seq (chromatin accessibility; red) of the tumors as in “A” (n = 2 mice per group). d Representative microscopic images of WTD and KOD tumor slides stained with anti-MYC antibody. n = 3 biological replicates. Scale bar, 100 µm. e Western blot analysis of WTD and KOD cells treated or untreated with rEndocan (10 ng/ml) for 3 days. Representative result of n = 3 biological replicates. f qRT-PCR analysis of MYC expression in control and rEndocan (10 ng/ml) or rPDGFBB (10 ng/ml) treated cells human GBM cells (1079 and 413 cell lines). ***P = 0.0005 for rEndocan vs. Control and ***P = 0.0005 for rPDGFBB vs. Control in 1079 cells. ****P < 0.0001 for rEndocan vs. Control and rPDGFBB vs. Control in 413 cells. n = 3 biological replicates, One-way ANOVA with Dunnett’s multiple comparisons test. g Western blot analysis for MYC and β- actin protein in 1079 cells treated with increasing doses of rEndocan for 72 h. Representative result of n = 3 biological replicates. Source data are available in the Source Data file.