Fig. 3
From: YTHDF1 targets the chemotherapy response by suppressing NOTCH1-induced stemness in colorectal cancer
Multiomic profiling identified NOTCH1 as a downstream target of YTHDF1. a Schematic of integrative MeRIP-seq, RNA-seq, and Ribo-seq. b MeRIP-seq of CSC28 revealed the normalized distribution of m6A peaks and identified m6A motifs. c Pathway enrichment analysis (GSEA-KEGG) of the top enriched genes among the MeRIP-seq data. d The m6A peak of NOTCH1 was located at the 3′ UTR. e RNA-seq revealed that NOTCH1 signaling was the most enriched pathway in YTHDF1-overexpressing CSC28 cells. f Schematic of overlapping MeRIP-seq, RNA-seq, and Ribo-seq. g Schematic of MeRIP-qPCR. h Schematic of RIP-qPCR. i Schematic of RNC-qPCR. j Level of m6A modification on NOTCH1 mRNA (N = 3 per group). k Levels of NOTCH1 mRNA in YTHDF1-overexpressing and YTHDF1-mutant CSCs (N = 3 per group). l Levels of NOTCH1 mRNA in the active RNC complex (N = 3 per group). m Relative NOTCH1 luciferase activity in YTHDF1 wild-type or mutant-overexpressing or YTHDF1-knockdown CSCs (N = 3 per group). n pmirGLO-NOTCH1-mutant reporters with mutated m6A sites (RRACH to TTTCT) in the 3′UTR. o Relative luciferase activities of the pmirGLO-NOTCH1 or pmirGLO-NOTCH1-mutant reporter in CSCs (N = 3 per group). The data are presented as the means ± SDs. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001; 2-tailed t-test (j, o), ordinary one-way ANOVA (k, l, m)
