Skip to main content

Advertisement

Fig. 3 | Clinical Epigenetics

Fig. 3

From: Co-inhibition of HDAC and MLL-menin interaction targets MLL-rearranged acute myeloid leukemia cells via disruption of DNA damage checkpoint and DNA repair

Fig. 3

RNA sequencing reveals genome-wide gene expression profiles of MOLM-13 cells treated with chidamide and MI-3 alone or in combination. a, b MOLM-13 cells were treated with 2.6 μM chidamide ± 13.9 μM MI-3 for 24 h (a) or 48 h (b), after which total RNA was extracted and subjected to whole exome RNAseq that was performed in triplicate for each condition. The KEEG analysis reveals the annotations of the most enriched pathways of differentially expressing genes after combined treatment for 48 h, compared to untreated control. c–e Alternatively, a Venn diagram shows the number of genes and their relationship that were differentially expressed (log2FC ≥ 1, Q value ≤ 0.001) after treatment with chidamide and MI-3 alone or in combination, compared to untreated control (c). A heatmap shows hierarchical clustering of 635 genes significantly affected by all three treatments, including chidamide, MI-3, and combined treatment (d). A heatmap shows hierarchical clustering of 59 genes (indicated by square in panel B) that were upregulated by chidamide and combined treatment, but downregulated by MI-3 (e). f Real-time PCR analysis was performed to monitor expression of IL1B, one of 59 genes shown in panel c, in MOLM-13 cells after treated with chidamide ± MI-3 for 48 h. The reaction was carried out in triplicate and relative expression levels were calculated as 2CT after normalization to β-actin. Values indicate mean ± SEM for at least three independent experiments performed in triplicate (**P < 0.01, NS = not significant)

Back to article page