The ECHS1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt ECHS1 in the human gastric cancer line HGC-27. This polyclonal model provides a genetically heterogeneous loss-of-function system, avoiding clonal selection artifacts. It is suitable for investigating ECHS1-dependent mitochondrial fatty acid oxidation in cancer metabolism, supporting applications such as metabolic flux analysis and functional genomics.
HGC-27 is a poorly differentiated gastric adenocarcinoma cell line derived from a lymph node metastasis. It serves as a widely used in vitro model for studying gastric cancer biology, including tumor progression, metastasis, and metabolic adaptations. The cell line exhibits hallmark characteristics of aggressive gastric cancer, such as rapid proliferation and altered energy metabolism. Its origin from a metastatic site makes it particularly relevant for investigating metabolic vulnerabilities that support cancer cell dissemination and survival under metabolic stress.
ECHS1 encodes mitochondrial short-chain enoyl-CoA hydratase, a key enzyme in the second step of fatty acid ??-oxidation. It catalyzes the hydration of short-chain enoyl-CoA to 3-hydroxyacyl-CoA, feeding into the production of acetyl-CoA, NADH, and FADH2, which fuel the TCA cycle and ATP generation. ECHS1 functions downstream of transcriptional regulators PPARA, PPARD, and PPARGC1A, which control fatty acid oxidation capacity in response to nutrient availability. It interacts with mitochondrial trifunctional protein components HADHA, HADHB, and auxiliary enzyme ECHDC1. Disruption of ECHS1 leads to accumulation of enoyl-CoA intermediates and reduced acetyl-CoA and ATP synthesis, impairing mitochondrial energy metabolism.
In the context of HGC-27 gastric cancer cells, ECHS1 knockout significantly impacts metabolic flexibility. Gastric cancer cells often rely on fatty acid oxidation for energy production, especially under glucose-limited conditions or during metastasis. Loss of ECHS1 disrupts the ??-oxidation pathway, forcing cells to depend more heavily on glycolysis or alternative substrates, and sensitizing them to metabolic stress. This model is therefore valuable for dissecting the role of mitochondrial fatty acid oxidation in cancer cell proliferation, survival, and adaptation to the tumor microenvironment, and for evaluating ECHS1 as a potential metabolic vulnerability in gastric cancer.
This polyclonal knockout product supports a variety of research applications, including metabolic disorder modeling, mitochondrial dysfunction studies, and fatty acid oxidation analysis. Researchers can employ representative assays such as Seahorse metabolic flux analysis to measure oxygen consumption rate, fatty acid oxidation assays using labeled palmitate, ATP bioluminescence assays, and lipidomics profiling to assess fatty acyl-CoA accumulation. Western blotting and RT-qPCR can confirm ECHS1 disruption. Additionally, cell viability assays under glucose deprivation or in the presence of fatty acid oxidation inhibitors can reveal metabolic dependencies. For detailed product specifications, technical support, or custom inquiries, please contact Ascent Research.
