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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: Super-enhancer profiling identifies novel critical and targetable cancer survival gene LYL1 in pediatric acute myeloid leukemia

Fig. 5

A The Hi-C data analysis of super-enhancer regions and promoter of LYL1 in THP-1 cell line (track 1) represents interaction at the LYL1 gene loci, and the ChIP-seq gene tracks (track 2–15) represent the H3K27ac signal in AML cell lines (NB4, MV4–11, and THP1) and 11 AML samples at the LYL1 gene loci. The super-enhancers are shown as green boxes. B The public BRD4 ChIP-Seq data of AML cell line MV4–11 (GSE101821) showed that the gene region of LYL1 had coincident signals (track 1). The ChIP-seq gene tracks represent the H3K27ac signal in NB4 cells (track 2) and NB4 cells treated with GNE-987 (25 nM, 24 h) (track 3) at the LYL1 gene loci. The reads signal of RNA-Seq in NB4 cells (track 4–5) and NB4 cells treated with GNE-987 (25 nM, 24 h) (track 6–7) at the LYL1 gene loci. C Western blotting showed that LYL1 level was significantly decreased in NB4 cells treated with GNE-987 (0, 1, 2, 6, 12 nM, 24 h). D Western blotting showed that LYL1 level was significantly decreased in Kasumi-1 cells treated with GNE-987 (0, 1, 2, 6, 12 nM, 24 h). E qPCR showed that LYL1 was significantly downregulated in NB4 cells treated with GNE-987 (0, 1, 2, 6, 12 nM, 24 h). F qPCR showed that LYL1 was significantly downregulated in Kasumi-1 cells treated with GNE-987 (0, 1, 2, 6, 12 nM, 24 h). G expression pattern of LYL1 between AML patients and healthy controls in public transcriptomic dataset (GSE114868)

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