The ECI1 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population with targeted disruption of the ECI1 gene in K-562 cells. This heterogeneous pool of edited cells is ideal for loss-of-function studies at the population level, enabling robust metabolic and genetic screening without clonal selection.
The parental K-562 cell line was established from the bone marrow of a CML patient in blast crisis. These BCR-ABL1-positive, undifferentiated hematopoietic blasts are a classic model for erythroleukemia and hematopoietic differentiation. Their well-characterized oncogenic signaling and metabolic adaptations make them suitable for studying metabolic dependencies in a leukemic context.
ECI1 encodes mitochondrial enoyl-CoA delta isomerase, which catalyzes the isomerization of 3-cis/trans-enoyl-CoA to 2-trans-enoyl-CoA, a prerequisite for complete ??-oxidation of unsaturated fatty acids. This reaction feeds into the enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase, and 3-ketoacyl-CoA thiolase cascade, ultimately generating acetyl-CoA, NADH, and FADH2. ECI1 is transcriptionally regulated by PPAR?? and PGC-1??, linking its expression to fasting, glucagon, and high-fat diet. Disruption of ECI1 blocks unsaturated fatty acid degradation, leading to reduced ATP and acetyl-CoA production and potential accumulation of lipotoxic intermediates.
In K-562 leukemic cells, ECI1 knockout allows investigation of how unsaturated fatty acid oxidation supports proliferation and survival in a BCR-ABL1-driven background. This model can reveal metabolic dependencies and test the therapeutic potential of targeting fatty acid oxidation with agents like etomoxir. It also enables studies on lipotoxicity and the interplay between lipid metabolism and oncogenic signaling.
Applications include metabolic flux assays with radiolabeled oleate, Seahorse analysis, lipidomics profiling, and drug sensitivity testing. Standard validation can be performed by western blot and RT-qPCR. The polyclonal format supports pooled screening and population-based functional assays. For additional information, please contact Ascent Research.
