ECH1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric adenocarcinoma AGS cell line, designed for disruption of the ECH1 gene. This product offers a loss-of-function model for studying enoyl-CoA hydratase 1 (ECH1) in mitochondrial fatty acid ??-oxidation. Because it comprises a heterogeneous pool of edited cells without single-cell cloning, it preserves the biological variability of a polyclonal population, suitable for initial functional screening and pathway analysis.
The AGS cell line is a widely used human gastric epithelial adenocarcinoma model, originally isolated from a patient with gastric cancer. These cells display characteristic features of gastric epithelium, including barrier formation and secretory activity, and serve as a valuable in vitro system for investigating gastric cancer cell biology, metabolism, and drug responses. Their robust growth and genetic tractability make them an ideal host for CRISPR-based genome editing to explore gene function in a gastric context.
ECH1 encodes a mitochondrial enzyme that catalyzes the hydration of enoyl-CoA intermediates to 3-hydroxyacyl-CoA, a key step in the ??-oxidation of unsaturated fatty acids. This reaction is essential for the complete degradation of these lipids, yielding acetyl-CoA for the tricarboxylic acid cycle and ATP production. Expression of ECH1 is regulated by the peroxisome proliferator-activated receptors PPARA and PPARG, transcription factors that orchestrate lipid catabolism. Within the mitochondrial ??-oxidation pathway, ECH1 functionally interacts with the trifunctional protein subunits HADHA and HADHB and operates downstream of long-chain acyl-CoA dehydrogenases such as ACADVL. Disruption of ECH1 impairs this pathway, reducing acetyl-CoA supply, mitochondrial respiration, and ATP synthesis, thereby perturbing cellular energy metabolism and lipid homeostasis.
Gastric adenocarcinoma cells often rewire lipid metabolism to support rapid proliferation and survival. ECH1 loss in AGS cells is predicted to compromise fatty acid oxidation, leading to accumulation of intermediates and metabolic stress. This model enables researchers to dissect how defects in mitochondrial ??-oxidation impact gastric tumor cell growth, lipid droplet dynamics, and adaptation to nutrient deprivation. The polyclonal knockout population, while not clonally pure, provides a cost-effective tool to observe dominant phenotypes and interrogate metabolic vulnerabilities that may be exploited therapeutically in gastric cancer and other metabolic disorders.
This product is well-suited for a variety of research applications. Fatty acid oxidation assays and Seahorse Mito Stress Tests can quantify the impact on mitochondrial respiration and overall metabolic flux. Lipidomic analyses reveal changes in lipid species profiles, while cell proliferation and viability assays address growth consequences. Target gene disruption can be confirmed by western blotting or RT-qPCR for ECH1. These approaches help identify metabolic dependencies and evaluate lipid metabolism-targeting strategies. For technical inquiries or ordering, please contact Ascent Research.
