ATGL suppresses ferroptosis in acute myeloid leukemia cells via modulating the CEBPa/SCD1 axis and induces gilteritinib resistance.
Metabolic reprogramming disrupts energy homeostasis and promotes tumor cell proliferation.  We here report PNPLA2/ATGL as a key regulator of lipid metabolism in progress of AML.The depletion of ATGL will slow the malignant progression of AM L through the plasma metabolic pathway.Our data provide transcriptional data from an AML in which ATGL is missing from the mass metabolism direction. Overall design: RNA-seq profiling of knockdown of ATGL on gene expression  of MV4-11 cells (shNC, shATGL)