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. 2021 Jul 13;11(17):8172–8184. doi: 10.7150/thno.56737

Figure 4.

Figure 4

Cpd-1 inhibited aberrant gene expression in MLL-r leukemia. (A, B) Treatment of (A) Molm-13 and (B) MV4;11 cells with Cpd-1 for 4 days dose-dependently suppressed expression of MLL target genes HoxA9, Meis1 and Myc (* p < 0.05). DOT1L inhibitor EPZ4777 behaved similarly, but inactive Cpd-3 had no activity. Data were from two or more experiments; (C) Similar to EPZ4777 (2 μM), treatment with Cpd-1 (5 μM for 4 days) caused decreased levels of H3K79me2 in the gene promoters of HoxA9 and Myc in Molm-13 cells (* p < 0.05); (D) Gene profiling followed by gene set enrichment analysis (GSEA) shows that treatment of Molm-13 cells with Cpd-1 (5 µM for 4 days) recapitulated activities of 1) DOT1L knockdown (GSE25911), 2) DOT1L inhibition by EPZ4777 (GSE29828), 3) MLL-AF9 knockdown (GSE36592), and 4) HoxA9 knockdown (GSE33518). It also significantly 5) upregulated HoxA9-downregulated target genes (GSE13714), and 6) downregulated Myc target genes (GSE32220).