The ECHDC1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma cell line HGC-27, designed to disrupt expression of the ECHDC1 gene. This product provides a heterogeneous pool of cells with targeted gene disruption, enabling functional studies of ECHDC1 in a gastric cancer background without clonal selection bias.
HGC-27 is a widely characterized human gastric carcinoma cell line originally isolated from a metastatic lymph node of a gastric adenocarcinoma patient. The cells exhibit an epithelial, adherent morphology and serve as a well-established in vitro model for studying gastric cancer biology, including tumor progression, signaling pathways, and metabolic reprogramming.
ECHDC1 encodes an enoyl-CoA hydratase that catalyzes the second step of the mitochondrial fatty acid ??-oxidation spiral, converting trans-2-enoyl-CoA to 3-hydroxyacyl-CoA. This enzyme functions as a component of the mitochondrial trifunctional protein (TFP) complex, interacting with HADHA, HADHB, and ACADVL. The expression and activity of ECHDC1 are positively regulated by nuclear receptors and coactivators such as PPARA, PPARG, and PGC-1??, as well as by SIRT1 and insulin signaling. Through its catalytic action, ECHDC1 contributes to the generation of acetyl-CoA, NADH, and FADH2, which feed into the tricarboxylic acid cycle and oxidative phosphorylation, thereby linking lipid metabolism to cellular energy status.
In the context of HGC-27 cells, ECHDC1 knockout is particularly relevant for investigating metabolic vulnerabilities in gastric cancer. Many cancer cells, including gastric carcinomas, rewire fatty acid metabolism to support proliferation and survival. Disruption of ECHDC1 impairs mitochondrial ??-oxidation, potentially sensitizing cells to metabolic stress and altering the balance between lipid synthesis and degradation. This model enables dissection of how fatty acid oxidation contributes to gastric cancer cell growth, resistance to nutrient deprivation, and response to pharmacological agents targeting metabolic pathways.
Researchers can employ these ECHDC1 Knockout HGC-27 Polyclonal Cells in a variety of applications, including Western blotting and RT-qPCR to confirm gene disruption and assess compensatory metabolic enzyme expression, enzyme activity assays and fatty acid oxidation rate measurements using radiolabeled or stable isotope-labeled substrates, Seahorse metabolic flux analysis to evaluate mitochondrial respiration and glycolytic capacity, metabolomics profiling to map changes in acyl-carnitines and TCA cycle intermediates, and colony formation assays to assess clonogenic survival under metabolic challenge. These functional studies facilitate drug screening for metabolic inhibitors and characterization of ECHDC1 as a target in gastric cancer. For technical assistance and ordering information, please contact Ascent Research.
