The ECHDC3 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma line. This product provides heterogeneous cells with targeted disruption of ECHDC3, enabling loss-of-function studies without clone isolation. The knockout suppresses mitochondrial enoyl-CoA hydratase activity in fatty acid ??-oxidation, suitable for population-level metabolic analyses.
The parental A2780 line is a well-characterized ovarian endometrioid adenocarcinoma model, adherent and p53 wild-type. It retains intact apoptotic signaling, critical for dissecting metabolic contributions to drug sensitivity. Its sensitivity to platinum agents and relevance in ovarian cancer progression make it ideal for studying fatty acid metabolism??s role in tumor survival and chemoresistance.
ECHDC3 encodes a mitochondrial enoyl-CoA hydratase catalyzing hydration of trans-2-enoyl-CoA to 3-hydroxyacyl-CoA, a rate-limiting step in fatty acid ??-oxidation. This reaction supplies acetyl-CoA, NADH, and FADH2 for the TCA cycle and ATP synthesis. Its expression is regulated by PPAR??/PPAR??, PGC-1??, and ERR??, and is modulated by AMPK/SIRT1 signaling. The enzyme interacts functionally with ECHS1, HADHA/HADHB, and various acyl-CoA dehydrogenases, integrating lipid oxidation with cellular energy homeostasis.
In A2780 cells, ECHDC3 knockout allows investigation of ovarian cancer metabolic reprogramming, where fatty acid oxidation often supports proliferation and drug resistance. Using a p53 wild-type background, researchers can isolate the impact of ??-oxidation on cisplatin sensitivity, lipid accumulation, and redox control. This model enables direct comparison of wild-type and ECHDC3-deficient cells to identify metabolic vulnerabilities specific to ovarian tumors.
Applications include Seahorse extracellular flux analysis and 14C-palmitate oxidation assays to measure metabolic flux, ATP luminescence assays for energy status, lipid droplet staining and LC-MS lipidomics for lipid profiling, and cell viability/apoptosis/migration assays under metabolic stress, including cisplatin sensitivity screens. Molecular validation by western blotting and RT-qPCR complements functional studies. This product supports research into ovarian cancer metabolism, mitochondrial dysfunction, and drug resistance. For further information, contact Ascent Research.
