The ECH1 Knockout K-562 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ECH1 gene in the human K-562 chronic myelogenous leukemia (CML) cell line. This product delivers a heterogeneous pool of edited cells with disrupted ECH1 gene expression, providing a versatile loss-of-function model for dissecting peroxisomal fatty acid beta-oxidation without the need for single-cell cloning. The polyclonal format captures the genetic diversity of the editing outcome, enabling robust population-level studies of metabolic pathways.
K-562 cells were originally derived from the pleural effusion of a 53-year-old female with CML in blast crisis and harbor the BCR-ABL oncogenic fusion. They display a near-triploid karyotype and serve as a widely used model for hematopoietic differentiation and leukemia biology. Their BCR-ABL-driven signaling imposes distinct metabolic demands, making them particularly valuable for investigating how lipid metabolism intersects with oncogenic pathways and contributes to leukemia cell fitness.
The ECH1 gene encodes enoyl-CoA hydratase 1, a peroxisomal enzyme that catalyzes the hydration of trans-2-enoyl-CoA to 3-hydroxyacyl-CoA, a critical step in the beta-oxidation of fatty acids. ECH1 functions within a multi-enzyme complex that includes ACOX1, HSD17B4, and ACAA1. Its expression is induced by PPAR?? agonists such as fatty acids and fibrates, placing it under nutrient-sensing transcriptional control. Disruption of ECH1 leads to accumulation of upstream fatty acyl-CoA intermediates and reduces production of acetyl-CoA, NADH, and FADH2, impairing cellular energy metabolism and lipid homeostasis.
In the context of K-562 leukemia cells, ECH1 knockout provides a powerful tool to study how peroxisomal beta-oxidation defects influence malignant phenotypes. Given the heightened metabolic activity and altered lipid metabolism in cancer cells, this model can reveal dependencies on fatty acid oxidation for proliferation and survival. It also offers insights into how BCR-ABL signaling interacts with peroxisomal function, potentially uncovering metabolic vulnerabilities that could be exploited therapeutically.
This knockout cell population is suited for a range of experimental applications, including validation of ECH1 disruption by Western blotting and RT-qPCR, functional analysis of fatty acid oxidation rates using labeled substrates, untargeted metabolomics to profile lipid intermediates, and drug sensitivity assays to assess altered responses to chemotherapeutics. Researchers can employ these cells to investigate peroxisomal disorders, metabolic reprogramming in leukemia, and the broader role of lipid catabolism in cancer. For additional information or to discuss custom applications, please contact Ascent Research.
