ECI2 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population engineered for disruption of the ECI2 gene in the A2780 human epithelial ovarian carcinoma cell line. This polyclonal knockout pool provides a heterogeneous loss-of-function system suitable for analyzing fatty acid metabolism, energy homeostasis, and cancer cell metabolic reprogramming without clonal selection or single-cell-derived lines. The knockout model is generated via CRISPR/Cas9-mediated gene disruption, yielding a mixed population of edited alleles that collectively abrogate ECI2 expression, enabling robust assessment of gene function in a cellular context representative of high-grade serous ovarian cancer.
The A2780 cell line was established from an untreated patient with ovarian endometrioid carcinoma and is widely employed as a model for ovarian cancer drug sensitivity and resistance studies. A2780 cells retain epithelial morphology and key oncogenic signaling features, making them a standard platform for investigating chemotherapeutic response, particularly to platinum-based agents and PARP inhibitors. Their utility in metabolic research is growing, given the emerging role of lipid metabolism in ovarian cancer progression and treatment resistance, positioning A2780 as a relevant host for ECI2 knockout studies.
ECI2 encodes enoyl-CoA delta isomerase 2, a mitochondrial auxiliary enzyme that catalyzes the isomerization of 3-cis and 3-trans double bonds in enoyl-CoA esters to the 2-trans form, a necessary step for the complete beta-oxidation of unsaturated fatty acids. This enzyme functions within the broader fatty acid beta-oxidation pathway, interacting with the trifunctional protein complex subunits HADHA and HADHB, as well as ECHS1, to sustain acetyl-CoA, NADH, and FADH2 production. Upstream regulators PPAR??, PGC-1??, and AMPK integrate metabolic signals to control ECI2 expression, linking nutrient sensing to lipid catabolism. Pathway components such as CPT1, ACOX1, and ACAA2 illustrate the multistep process in which ECI2 acts at the level of enoyl-CoA isomerization, ensuring efficient energy extraction from dietary and endogenous unsaturated lipids.
In the A2780 ovarian cancer background, ECI2 knockout is anticipated to impair mitochondrial unsaturated fatty acid oxidation, forcing metabolic adaptation or reducing bioenergetic capacity. Given that many cancer cells, including ovarian carcinomas, rely on fatty acid oxidation for survival under stress or during metastasis, ECI2 disruption may reveal vulnerabilities in lipid-dependent energy production. This model enables dissection of how ECI2 loss alters acetyl-CoA pools, NADH/NAD+ ratios, and lipid droplet dynamics, offering insights into metabolic liabilities that could be targeted therapeutically. Additionally, because A2780 cells are commonly used in drug sensitivity assays, this knockout system can illuminate how fatty acid oxidation status influences response to standard-of-care chemotherapies.
Typical research applications include metabolic flux analysis, fatty acid oxidation assays, cell viability and proliferation studies, and drug sensitivity profiling. Researchers may employ western blotting and RT-qPCR to confirm ECI2 disruption and assess compensatory pathway activation. The polyclonal nature permits studying population-level metabolic heterogeneity. This product is ideal for investigating cancer metabolism, metabolic disorders, and the role of lipid utilization in drug resistance. For further details or ordering information, please contact Ascent Research.
