The EHHADH Knockout A2780 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population of human A2780 ovarian carcinoma cells with targeted disruption of the EHHADH gene. This product provides a loss-of-function model without clonal isolation, enabling study of collective gene ablation effects in a tumorigenic epithelial setting.
A2780 is an established human ovarian carcinoma cell line derived from an untreated patient, serving as a standard tumor model. These tumorigenic cells are widely used to investigate ovarian cancer biology, metabolic reprogramming, and therapeutic responses.
EHHADH encodes a bifunctional enzyme possessing both enoyl-CoA hydratase and 3-hydroxyacyl-CoA dehydrogenase activities, catalyzing the second and third reactions in peroxisomal fatty acid beta-oxidation. This enzyme acts downstream of the transcription factor PPARA, which is activated by ligands such as fenofibrate. Within the peroxisomal oxidation cascade, EHHADH functions after the transporter ABCD1 and the oxidase ACOX1, and in concert with HSD17B4 and SCP2, driving the conversion of fatty acyl-CoAs to acetyl-CoA and NADH. Its peroxisomal localization depends on interaction with the receptor PEX5. By disrupting EHHADH, the breakdown of very long-chain and branched-chain fatty acids is compromised, leading to lipid accumulation and metabolic dysregulation.
In the A2780 ovarian carcinoma model, EHHADH knockout provides a valuable tool to explore how peroxisomal lipid metabolism supports cancer cell fitness. Ovarian cancer cells often exhibit altered fatty acid utilization, and loss of EHHADH may induce compensatory shifts toward mitochondrial oxidation or lipogenesis. This polyclonal knockout system can be used to study the impact on cell proliferation, redox homeostasis, and signaling pathways linked to PPAR??. Coupling the knockout with lipidomic profiling or metabolomic analyses enables detailed characterization of metabolic vulnerabilities in ovarian cancer.
This polyclonal knockout model is suitable for western blotting and RT-qPCR to validate gene disruption, peroxisomal beta-oxidation assays to assess functional consequences, immunofluorescence for peroxisomal markers, and cell proliferation assays under defined lipid conditions. It can also be used in xenograft models to examine tumor dependency on peroxisomal fatty acid oxidation. For further information, please contact Ascent Research.
