The ECI1 Knockout AGS Polyclonal Cells constitute a polyclonal population of human gastric adenocarcinoma epithelial cells in which the ECI1 gene has been disrupted using CRISPR/Cas9-mediated gene editing. This product provides a pooled loss-of-function model for investigating the role of the mitochondrial enzyme enoyl-CoA delta isomerase 1 in fatty acid metabolism within a well-characterized gastric cancer background. The polyclonal format captures a heterogeneous mix of targeted alleles, enabling robust, population-level studies of ECI1-dependent phenotypes without clonal selection bias.
The host cell line, AGS, was derived from a poorly differentiated gastric adenocarcinoma isolated from a 54-year-old Caucasian female and is widely employed as a model epithelial cell line for gastric cancer biology and preclinical drug testing. AGS cells exhibit key features of gastric adenocarcinoma, including aberrant signaling pathways and metabolic reprogramming, making them a suitable platform for dissecting connections between lipid metabolism and oncogenic processes. Their epithelial origin and established use in cancer research provide a physiologically relevant context for functional genomic studies.
ECI1 encodes a mitochondrial enzyme that catalyzes the isomerization of 3-cis and 2-trans enoyl-CoA esters, a necessary step for the complete beta-oxidation of unsaturated fatty acids. This reaction feeds into the broader mitochondrial fatty acid oxidation pathway, working in concert with carnitine shuttle enzymes such as CPT1 and CPT2, acyl-CoA dehydrogenases like ACADVL, and the trifunctional protein subunits HADHA and HADHB. ECI1 is transcriptionally regulated by the nuclear receptors PPARA and PPARD, which are themselves influenced by AMPK signaling. The enzyme interacts directly with ECHS1 and forms functional complexes with other beta-oxidation components to generate acetyl-CoA, NADH, FADH2, and ATP. Disruption of ECI1 thus impairs efficient lipid catabolism, perturbing cellular energy homeostasis and downstream lipid-derived signaling pathways.
In AGS gastric cancer cells, ECI1 knockout creates a unique experimental system to examine how attenuated fatty acid oxidation reshapes metabolic dependencies and tumor cell adaptation. Gastric adenocarcinomas frequently exhibit altered lipid uptake, storage, and utilization; loss of enoyl-CoA isomerase activity may force reliance on alternative energy substrates or unmask vulnerabilities that can be exploited therapeutically. This model allows researchers to interrogate the interplay between mitochondrial beta-oxidation, oncogenic signaling networks, and the tumor microenvironment, potentially revealing new mechanisms of metabolic cardiomyopathy-like stress responses or enoyl-CoA isomerase deficiency-related phenotypes in a cancer-relevant context.
The ECI1 Knockout AGS Polyclonal Cells are ideally suited for metabolic profiling in gastric cancer research, including oxygen consumption measurement by Seahorse metabolic flux analysis, acylcarnitine profiling by mass spectrometry, and ATP bioluminescence assays. They also support drug screening for fatty acid oxidation inhibitors and assessment of cell viability under lipid-rich conditions, enabling biomarker discovery and functional validation of metabolic targets. For further inquiries or to request additional product information, please contact Ascent Research.
