The ECH1 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma cell line, featuring targeted disruption of the ECH1 gene using CRISPR/Cas9 technology. This product provides a heterogeneous pool of cells with loss-of-function mutations in enoyl-CoA hydratase 1, enabling functional studies of this enzyme in a gastric cancer model.
The HGC-27 cell line originates from the lymph node metastasis of a poorly differentiated gastric adenocarcinoma and exhibits epithelial morphology. It is widely used to investigate mechanisms of gastric cancer progression, metastatic dissemination, and metabolic reprogramming, making it an ideal host for studying the role of fatty acid metabolism in tumor biology.
ECH1 encodes enoyl-CoA hydratase 1, a peroxisomal and mitochondrial enzyme that catalyzes the isomerization of 3,5-dienoyl-CoA to 2,4-dienoyl-CoA during ??-oxidation of unsaturated fatty acids. This reaction is essential for complete fatty acid degradation to acetyl-CoA, which fuels the TCA cycle and ATP production. ECH1 is transcriptionally regulated by PPAR?? and PGC-1??, integrating signals from nutrient availability and insulin/glucagon signaling. The enzyme interacts with the peroxisomal targeting signal receptor and cooperates with HSD17B4 and ACAA1 to process unsaturated fatty acids, generating 2,4-dienoyl-CoA that is subsequently reduced by 2,4-dienoyl-CoA reductase. This pathway produces NADH and FADH2, linking fatty acid oxidation to mitochondrial oxidative phosphorylation.
In HGC-27 gastric cancer cells, loss of ECH1 function is predicted to impair the oxidation of unsaturated fatty acids, potentially disrupting energy homeostasis and biosynthetic precursor supply. As gastric cancer cells often upregulate fatty acid oxidation to support growth and metastasis, this knockout model offers a powerful tool for dissecting the contribution of auxiliary ??-oxidation enzymes to tumor metabolism and identifying metabolic dependencies that could be exploited therapeutically.
This polyclonal knockout model supports diverse experimental approaches, including western blotting to confirm ECH1 depletion, radiolabeled palmitate oxidation assays to measure fatty acid flux, and acylcarnitine profiling to assess ??-oxidation activity. It is suitable for proliferation assays under metabolic stress, functional genomics screens, drug targeting of lipid metabolism, and transcriptomic analyses such as RNA-seq to explore compensatory pathways. For further information, please contact Ascent Research.
