Fig. 4: RUNX1 interacts with NPM1 to allow the chromatin accessibility and promote FOSL2-mediated expressions of ECM-related genes. | Cell Death & Disease

Fig. 4: RUNX1 interacts with NPM1 to allow the chromatin accessibility and promote FOSL2-mediated expressions of ECM-related genes.

From: RUNX1/NPM1/H3K4me3 complex contributes to extracellular matrix remodeling via enhancing FOSL2 transcriptional activation in glioblastoma

Fig. 4: RUNX1 interacts with NPM1 to allow the chromatin accessibility and promote FOSL2-mediated expressions of ECM-related genes.

A Schematic diagram of the single-cell ATAC-sequencing in N9 cells transfected with shVector or shRUNX1. B Clustering results of N9-shVector or shRUNX1 cells based on the ATAC-sequencing data were visualized as a tSNE plot. C Peak distribution analysis of RUNX1-associated chromatin regions in N9 cells transfected with shVector or shRUNX1. D Differential accessibility analysis in RUNX1 KD N9 cells was performed. E GO results of unique genes in N9-shVector cells. F Motif analysis and transcription factor prediction using RUNX1 ChIP-sequencing data. GI The mRNA, protein, and secretion levels of FOSL2, FN1, COL4A1, and LUM were measured by qRT-PCR, WB and ELISA assays in N9 cells transfected with siNC or siFOSL2. GAPDH served as the internal control. JL qRT-PCR, WB and ELISA results of the expression and secretion levels of RUNX1, FOSL2, FN1, COL4A1, and LUM in U-87 MG-LvVector, U-87 MG-LvRUNX1, or U-87 MG-LvRUNX1+siFOSL2 treated groups. GAPDH was used as the internal control. M, N ChIP-qRT-PCR results of FOSL2 occupying the promoter regions of ECM-related genes in N9 cells with RUNX1 or NPM1 KD. Student’s t-test for the two-group, and one-way ANOVA for comparisons of multiple groups. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

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