The ECHDC3 Knockout HGC-27 Polyclonal Cells product provides a ready-to-use, CRISPR/Cas9-edited polyclonal knockout cell population for investigating the function of the ECHDC3 gene in human gastric carcinoma. These polyclonal knockout cells, derived from the HGC-27 host cell line via targeted gene disruption, offer a stable loss-of-function model that eliminates the need for transient gene silencing, enabling immediate phenotypic analysis of ECHDC3 deficiency.
The host HGC-27 cell line is a well-characterized human gastric carcinoma epithelial model established from the lymph node metastasis of an undifferentiated gastric adenocarcinoma. It retains the aggressive growth properties and key metabolic features of undifferentiated gastric cancer, making it a suitable platform for studying the metabolic dependencies that support tumor proliferation and survival, particularly within the context of fatty acid metabolism and mitochondrial function.
ECHDC3 encodes an enoyl-CoA hydratase that catalyzes the hydration of enoyl-CoA esters in the mitochondrial fatty acid ??-oxidation pathway. The enzyme is transcriptionally regulated by PPAR?? and insulin, responding to fatty acid availability and hormonal status, and it physically interacts with the ?? and ?? subunits of the mitochondrial trifunctional protein, HADHA and HADHB. Functional loss of ECHDC3 disrupts the ??-oxidation cycle, leading to reduced acetyl-CoA production, attenuated AMPK signaling, and accumulation of lipid intermediates, as evidenced by increased Oil Red O staining. The pathway includes the upstream short-chain acyl-CoA dehydrogenase (ACADS) and the downstream hydroxyacyl-CoA dehydrogenase (HADH) and acetyl-CoA acetyltransferase (ACAT1), which work in concert to degrade fatty acids.
In HGC-27 gastric carcinoma cells, ECHDC3 knockout forces a metabolic shift from lipid utilization to alternative substrates such as glucose and glutamine, impairing cell proliferation under nutrient-limited conditions that mimic the tumor microenvironment. This metabolic vulnerability highlights the importance of fatty acid oxidation in supporting the energy and biosynthetic needs of undifferentiated gastric cancer, making the model valuable for studying the interplay between lipid metabolism, metabolic stress resistance, and oncogenic signaling.
Researchers can use these cells for fatty acid oxidation assays with radiolabeled palmitate, mitochondrial stress testing via Seahorse analysis, and cell proliferation or apoptosis assays under metabolic stress. The polyclonal knockout population is also suited for high-throughput metabolic inhibitor screens, multi-omics metabolomics and lipidomics profiling, and complementation studies to rescue ECHDC3 function. For further information or to place an order, please contact Ascent Research.
