ACSL4-Associated Lipid Metabolism is a Distinct Therapeutic Vulnerability in KMT2A-Rearranged Acute Myeloid Leukemia
We were interested in transcriptional changes after depletion of the lipid metabolic gene Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) in human acute myleoid leukemia (AML) cell lines. We compared global alterations of gene expression upon ACSL4 knockdown in one AML cell line harboring a lysine methyltransferase 2A (KMT2A) gene rearrangement (NOMO1) and one KMT2A WT AML cell line (K562). Overall design: RNA-Sequencing from NOMO1/K562 cells stably expressing dCas9-KRAB-GFP after transduction with either a sgRNA against a non-targeting control (NTC) or human ACSL4. Experiment was performed in biologically independent triplicates.