ECHDC3 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian cancer cell line. This product offers a heterogeneous pool of cells with targeted disruption of the ECHDC3 gene, which encodes a mitochondrial enoyl-CoA hydratase essential for fatty acid beta-oxidation. The polyclonal format avoids clonal selection bias, allowing researchers to study gene function in a cell population context relevant to cancer biology.
The MES-OV cell line originates from human ovarian adenocarcinoma and serves as a well-characterized epithelial ovarian cancer model. It is extensively used to investigate tumor biology, metastasis, and therapeutic responses, providing a physiologically relevant platform for studying metabolic adaptations in cancer. Its epithelial origin and oncogenic properties make it suitable for examining how lipid metabolism contributes to ovarian cancer progression.
ECHDC3 catalyzes the hydration of enoyl-CoA to 3-hydroxyacyl-CoA, a key reaction in mitochondrial fatty acid beta-oxidation. This enzyme operates downstream of transcriptional regulators such as PPARalpha, PPARgamma, and PGC-1alpha, which modulate lipid catabolism in response to insulin and glucagon signaling. ECHDC3 activity yields acetyl-CoA, NADH, and ATP, feeding the TCA cycle and oxidative phosphorylation. It interacts with beta-oxidation partners including ECHS1, HADHA, HADHB, and electron transfer flavoprotein (ETF), forming part of the mitochondrial trifunctional protein complex. Disruption of ECHDC3 impairs enoyl-CoA processing, leading to reduced fatty acid oxidation, altered lipid homeostasis, and decreased mitochondrial respiration.
In ovarian cancer cells, lipid metabolism is often reprogrammed to sustain rapid proliferation and resist apoptosis. Knockout of ECHDC3 in MES-OV cells disrupts this metabolic rewiring, creating a valuable model to study how impaired fatty acid oxidation impacts tumor cell viability, redox balance, and sensitivity to chemotherapeutics. The polyclonal nature captures the range of knockout phenotypes within a cancer cell population, mirroring the heterogeneity of metabolic vulnerabilities in tumors.
This knockout model is suited for a variety of functional assays, including Seahorse analysis of fatty acid oxidation, lipidomic profiling, mitochondrial respiration measurements, and ROS detection. It enables RT-qPCR and western blotting validation of metabolic gene expression changes, as well as cell proliferation and drug sensitivity screens. By elucidating the role of ECHDC3 in ovarian cancer metabolism, researchers can explore new therapeutic targets and biomarker opportunities. For further information, please contact Ascent Research.
