Effect of SGF29 deletion on H3K9 acetylation and antileukemia activity in human AML cells. (A) Volcano plot indicating changes in H3K9 acetylation peaks in U937 cells upon SGF29 deletion. Dots represent loci with significantly decreased (blue), increased (red), or unchanged (gray) acetylation peaks. Key SGF29-dependent AML oncogenes are labeled and (B) IGV tracks are shown for a subset of loci for SGF29 and SGF29 D196R mutant binding, H3K9ac and normalized RNA-seq transcript reads in the SGF29 wild-type and knockout (KO) conditions. (C) Venn diagram showing the overlap between SGF29 bound genes (yellow), genes downregulated upon SGF29 KO in RNA-seq (gray), and those that also lost promoter-associated H3K9ac (blue) are shown, and key AML oncogenes in the overlap are listed in the left panel. Right panel shows Metascape enrichment of gene ontology categories of the 882 genes common to all 3 sets. (D) Percentages of PDX AML-393 cells (x-axis) expressing an SGF29-targeting sgRNA (blue, BFP⁺) compared with untransduced cells (BFP⁻) over time in vitro. Progressive change in the percentage of BFP⁺ cells is shown at indicated time points on the y-axis. (E) Relative expression, as measured by quantitative real-time-PCR, of HOXA9 and MEIS1 in SGF29-deleted PDX AML-393 cells (y-axis) normalized to the NTC control is shown (n = 3). P values: ∗∗P < .05, ∗∗∗P < .01. (F) Kaplan-Meier survival curves for mice injected with NTC-sgRNA1 (black) or SGF29-sgRNA1 (blue) expressing PDX AML-393 (MLL-AF10 positive). Four mice were injected per group.