ECI2 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population in which the ECI2 gene has been disrupted in the MES-OV human ovarian endometrioid carcinoma cell line. This polyclonal knockout model provides a heterogeneous pool of cells harboring diverse editing events, enabling functional studies of ECI2 loss without clonal selection bias. The product is supplied as a growing population of adherent cells, suitable for immediate expansion and experimental use in metabolic and oncological research.
The MES-OV host cell line is derived from a human ovarian endometrioid carcinoma and retains wild-type TP53 status, making it a physiologically relevant model for studying ovarian cancer metabolism and signaling. These adherent cells exhibit epithelial morphology and have been extensively used to investigate cancer cell biology, including metabolic reprogramming and therapeutic responses. The TP53 proficiency distinguishes MES-OV from many commonly used ovarian cancer lines, allowing dissection of p53-dependent and -independent metabolic pathways.
ECI2 encodes mitochondrial enoyl-CoA delta isomerase, an auxiliary enzyme of fatty acid ??-oxidation. It isomerizes 3-cis and 3-trans double bonds in unsaturated fatty acyl-CoA intermediates to the 2-trans form required for subsequent steps by the trifunctional protein (HADHA/HADHB) and medium-chain acyl-CoA dehydrogenase (ACADM). ECI2 operates within a mitochondrial complex that includes very long-chain acyl-CoA dehydrogenase (ACADVL), electron transfer flavoproteins (ETFA, ETFB), and long-chain enoyl-CoA hydratase (ECI1). Its expression is regulated by PPAR?? and PPAR?? transcription factors, which respond to AMPK signaling, fasting, and high-fat diet. Downstream, ECI2 activity produces acetyl-CoA, NADH, and FADH2, fueling the TCA cycle and oxidative phosphorylation while modulating reactive oxygen species. CRISPR/Cas9 disruption of ECI2 impairs isomerization of unsaturated fatty acyl-CoA, causing accumulation of partially oxidized lipids and diminished acetyl-CoA output, thereby disrupting energy homeostasis.
In the MES-OV ovarian cancer context, ECI2 knockout creates a model system to test the dependence of endometrioid carcinoma cells on fatty acid ??-oxidation. Given that many cancers upregulate lipid metabolism to support proliferation and survival, ECI2 loss may uncover metabolic vulnerabilities specific to this tumor subtype. Coupled with the wild-type TP53 background, this model enables investigation of how p53 signaling intersects with mitochondrial fatty acid oxidation. Moreover, ECI2 knockout cells can be used to assess the efficacy of pharmacological inhibitors targeting fatty acid oxidation, such as etomoxir, providing a platform for preclinical metabolism-targeted therapy studies.
Typical research applications include elucidating the role of unsaturated fatty acid oxidation in ovarian cancer metabolic reprogramming, identifying synthetic lethal interactions, and evaluating sensitivity to FAO inhibitors. Representative assays include western blotting and RT-qPCR for ECI2 verification; Seahorse extracellular flux analysis to measure OCR and ECAR; [U-13C]palmitate tracing with LC-MS metabolomics; cell proliferation assays (MTT/EdU); lipid droplet staining (BODIPY); and flow cytometry for ROS detection. For further information, please contact Ascent Research.
