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Fig. 3 | Genome Medicine

Fig. 3

From: PRMT1-mediated H4R3me2a recruits SMARCA4 to promote colorectal cancer progression by enhancing EGFR signaling

Fig. 3

Identification of transcriptional targets of PRMT1 and SMARCA4. a,b Gene set enrichment analysis (GSEA) plots for cell proliferation-related and EGFR signaling pathway-related genes in HCT116 cells following PRMT1 knockdown (a) or SMARCA4 knockdown (b). c Quantitative real-time PCR analysis of PRMT1, TNS4, or EGFR mRNA levels normalized to GAPDH in scrambled negative control HCT116 cells (NC) and PRMT1-KD1/2 or SMARCA4-KD1/2 HCT116 cells. d Western blot analysis of indicated proteins in NC, PRMT-KD, and SMARCA4-KD HCT116 cells. Hsp70 served as a loading control. Data are representative of three independent experiments. e,f ChIP analysis of H4R3me2a and SMARCA4 binding to the TNS4 and EGFR promoter in NC, PRMT-KD, and SMARCA4-KD HCT116 cells. g ChIP-reChIP analysis of chromatin from HCT116 cells. The first antibody (H4R3me2a) and second antibody (SMARCA4) used in the reChIP are shown below the bar plot. The amount recovered from the reChIP was determined by qPCR and is shown as a percentage of the input. h ChIP analysis of SMARCA4 on the TNS4 and EGFR promoter from PRMT1 knockdown cells or NC control cells. i ChIP analysis of SMARCA4 on the TNS4 and EGFR promoter from PRMT1-Δ-overexpressing cells or EV (empty vector, MSCV) control cells. j Genomic tracks of ATAC and ChIP intensities of SMARCA4, H3K4me1, H3K4me3, and H3K27ac in the vicinity of TNS4 and EGRF loci in HCT116 cells. Track height is normalized to relative number of mapped reads. All results are shown as mean ± s.d. from three independent experiments. **P < 0.01 or *P < 0.05 compared to NC control or the indicated control (rabbit IgG)

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