The DECR2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human AGS gastric epithelial cell line. This heterogeneous knockout model supports parallel loss-of-function studies of DECR2 without clonal selection, providing a pooled background for investigating gene function in gastric biology.
The AGS cell line, originating from a human gastric adenocarcinoma, is a well-characterized adherent epithelial model for gastric cancer and infection research. AGS cells are extensively used to examine cellular metabolism, signal transduction, and host-pathogen interactions, and they offer a relevant platform for studying the role of fatty acid oxidation in gastric cancer progression.
DECR2 codes for 2,4-dienoyl-CoA reductase, which catalyzes the NADPH-dependent reduction of 2,4-dienoyl-CoA to trans-3-enoyl-CoA, an essential step for beta-oxidation of polyunsaturated fatty acids with even-numbered double bonds. This enzyme operates within the peroxisomal unsaturated fatty acid degradation pathway, which includes acyl-CoA oxidase, enoyl-CoA hydratase, 3-hydroxyacyl-CoA dehydrogenase, and beta-ketothiolase. DECR2 expression is controlled by the nuclear receptors PPAR??, PPAR??, and RXR, responding to fatty acid levels and insulin/glucagon signaling. The metabolic products acetyl-CoA, NADH, and FADH2 subsequently enter the TCA cycle and ketogenesis. Within the lipid catabolic network, DECR2 directly utilizes NADPH and 2,4-dienoyl-CoA and functionally cooperates with the mitochondrial trifunctional protein complex to maintain efficient energy extraction from unsaturated fatty acids.
In AGS gastric cancer cells, DECR2 knockout disrupts the complete degradation of unsaturated fatty acids, potentially leading to altered lipid utilization, impaired energy production, and disturbed cellular homeostasis. This disruption may impact metabolic reprogramming, redox status, and proliferation under lipid-rich conditions, offering a model to dissect how peroxisomal beta-oxidation contributes to gastric tumor biology and to identify metabolic vulnerabilities.
Typical applications include studying fatty acid metabolism in gastric cancer, metabolic reprogramming, peroxisomal biology, and drug target discovery. Phenotypic readouts rely on western blotting, RT-qPCR, Seahorse fatty acid oxidation assays, acylcarnitine profiling, NADPH/NADP+ ratio measurement, and cell proliferation assays under lipid-rich conditions, as well as direct 2,4-dienoyl-CoA reductase activity determination. These polyclonal knockout cells provide a flexible tool for exploring lipid-mediated signaling and metabolic disorders. Please contact Ascent Research for further details.
