The ECI1 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of MES-OV cells carrying targeted disruptions in the ECI1 gene. This knockout model provides a versatile tool for loss-of-function studies of enoyl-CoA delta isomerase 1, enabling population-level analyses of metabolic phenotypes without clonal selection bias. The polyclonal format captures the diversity of gene editing outcomes, making it ideal for assays that require averaged functional readouts such as metabolic flux and cell growth measurements.
The MES-OV cell line is a human epithelial ovarian adenocarcinoma model derived from a patient tumor. It is extensively used in ovarian cancer research to study tumorigenesis, metabolic reprogramming, and drug resistance mechanisms. The epithelial origin and molecular characteristics of MES-OV render it a clinically relevant platform for investigating the role of fatty acid oxidation in high-grade serous ovarian carcinoma, the most common and aggressive subtype.
ECI1 encodes mitochondrial enoyl-CoA delta isomerase 1, essential for isomerization of unsaturated enoyl-CoA esters during fatty acid ??-oxidation. This enzyme acts within a multienzyme complex that includes HADHA, HADHB, ACADVL, and the electron transfer proteins ETF and ETF-dehydrogenase, ultimately producing acetyl-CoA, NADH, and FADH2. Transcription of ECI1 is positively regulated by PPARA, PPARG, and HNF4A, and is modulated by the NAD+-dependent deacetylase SIRT1. In the broader ??-oxidation pathway, ECI1 functions downstream of CPT1A and CPT2 and cooperates with ECHS1 and HSD17B10. Disruption of ECI1 blocks the complete oxidation of unsaturated fatty acids, leading to accumulation of stalled intermediates and perturbed energy homeostasis.
In ovarian cancer, upregulation of fatty acid oxidation supports bioenergetic and biosynthetic demands, especially under nutrient stress. ECI1 knockout in MES-OV cells cripples utilization of unsaturated lipids, forcing metabolic rewiring and potentially exposing vulnerabilities for therapeutic targeting. The interplay with upstream regulators PPARA, PPARG, and SIRT1 makes this model valuable for dissecting how transcriptional control of lipid catabolism influences ovarian cancer aggressiveness and chemoresistance. This knockout model thus provides a powerful tool to investigate metabolic dependencies in ovarian adenocarcinoma.
Researchers can use these polyclonal knockout cells in fatty acid oxidation assays, Seahorse metabolic flux analysis, metabolomic profiling, and drug sensitivity testing under lipid-rich conditions. RT-qPCR and Western blot analyses of ECI1 and interacting partners such as HADHA and ACADVL are supported, alongside proliferation and apoptosis assays upon metabolic stress. For further technical details or custom cell engineering inquiries, contact Ascent Research.
