The ECH1 Knockout NCI-H1299 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the NCI-H1299 human non-small cell lung adenocarcinoma cell line. This product enables loss-of-function studies of ECH1, which encodes an enoyl-CoA hydratase critical for fatty acid ??-oxidation. The polyclonal format provides a heterogeneous mixture of edited alleles, facilitating population-level analyses of gene disruption effects on metabolic and oncogenic phenotypes.
NCI-H1299 cells are a widely used model of non-small cell lung cancer, originally established from a metastatic lymph node of a lung adenocarcinoma patient. These adherent epithelial cells lack expression of p53 protein and harbor other genomic alterations characteristic of advanced lung cancer, making them a suitable platform for investigating tumor metabolism and therapy resistance.
ECH1 encodes an enoyl-CoA hydratase that converts trans-2-enoyl-CoA to 3-hydroxyacyl-CoA in both mitochondrial and peroxisomal fatty acid ??-oxidation. The enzyme interacts with AUH, HADHA, HADHB, and PARK7, and functions within a multienzyme complex that includes ACADVL, HADHA, HADHB, HADH, and ACAA2. Its expression is transcriptionally regulated by nuclear receptors PPAR?? and PPAR??, as well as coactivator PPARGC1A and hypoxia-inducible factor HIF-1??. ECH1 activity yields acetyl-CoA, NADH, and FADH2, which fuel the TCA cycle and oxidative phosphorylation, and influence mTORC1 signaling.
Disruption of ECH1 in the NCI-H1299 background is predicted to impair ??-oxidation, reducing the supply of lipid-derived carbon for anabolism and energy production. This metabolic alteration could compromise tumor cell proliferation under nutrient-limited conditions or during anchorage-independent growth, and may increase sensitivity to metabolic inhibitors. As lung adenocarcinoma often displays altered fatty acid metabolism, this knockout model provides a valuable tool to dissect the contribution of ECH1 to cancer metabolic reprogramming.
This polyclonal ECH1 knockout cell population is suitable for a range of applications in metabolic oncology, including functional genomics screens, fatty acid oxidation assays using 14C-palmitate, and Seahorse metabolic flux analysis to measure oxygen consumption and extracellular acidification rates. It can be employed to validate ECH1 as a therapeutic target, study drug metabolism pathways, and identify synthetic lethal interactions in non-small cell lung cancer. End-point analyses such as Western blotting of ECH1 protein, RT-qPCR of ECH1 mRNA, and cell proliferation (MTT) or apoptosis (Annexin V) assays provide robust readouts for phenotypic characterization. For further details, please contact Ascent Research.
