The ECI1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 ovarian carcinoma cell line. This product features disruption of the ECI1 gene, which encodes the mitochondrial enoyl-CoA isomerase, a critical enzyme in the beta-oxidation of unsaturated fatty acids. The polyclonal nature of the knockout population provides a genetically heterogeneous model system, avoiding potential clonal artifacts while enabling robust studies of ECI1 loss-of-function effects on cellular metabolism.
The A2780 cell line was established from an untreated patient with ovarian endometrioid adenocarcinoma and serves as a well-characterized epithelial ovarian carcinoma model. These cells exhibit typical features of ovarian cancer, including dysregulated proliferation and metabolic adaptations that support tumor growth. The A2780 background is particularly relevant for investigating metabolic vulnerabilities in ovarian cancer, as these cells rely on mitochondrial oxidative metabolism, including fatty acid oxidation, for energy production and survival. This makes them an ideal host for studying the impact of ECI1 disruption on cancer cell metabolism.
ECI1 is a mitochondrial enzyme that catalyzes the isomerization of 3-cis- and 2-trans-enoyl-CoA intermediates derived from unsaturated fatty acids, enabling their complete degradation through beta-oxidation. The enzyme functions downstream of PPAR-alpha and PGC-1alpha, key transcriptional regulators of mitochondrial biogenesis and fatty acid oxidation, and its expression is activated by these factors. ECI1 interacts with the mitochondrial trifunctional protein complex (HADHA/HADHB), enoyl-CoA hydratase, and hydroxyacyl-CoA dehydrogenase to channel intermediates through the beta-oxidation spiral. Its enzymatic activity ultimately contributes to the production of acetyl-CoA, NADH, and ATP, fueling the tricarboxylic acid cycle and oxidative phosphorylation.
In the A2780 epithelial ovarian carcinoma model, knockout of ECI1 disrupts the complete breakdown of unsaturated fatty acids, leading to the accumulation of partially oxidized intermediates and a significant reduction in mitochondrial ATP production. This metabolic perturbation forces cells to rewire their energy metabolism, potentially increasing reliance on glycolysis or glutaminolysis. The model thus offers a powerful system to dissect metabolic reprogramming mechanisms in ovarian cancer, including adaptive responses to impaired fatty acid oxidation and the identification of synthetic lethal interactions that could be exploited therapeutically.
This polyclonal knockout product is ideally suited for a variety of research applications, including studies of fatty acid oxidation defects, metabolic reprogramming in cancer, and drug sensitivity profiling targeting mitochondrial metabolism. Representative assays include ATP production measurements, oxygen consumption rate (OCR) analysis, fatty acid oxidation flux assays, western blotting for ECI1 and related enzymes, metabolite profiling via mass spectrometry, mitochondrial isolation and enzyme activity assays, and cell viability assessments under metabolic stress conditions. For further information or to discuss customized applications, please contact Ascent Research.
