This product is a CRISPR/Cas9-edited polyclonal ECHS1 knockout cell population derived from the AGS human gastric adenocarcinoma epithelial cell line. The knockout has been generated through CRISPR/Cas9-mediated disruption of the ECHS1 gene, resulting in a heterogeneous population of cells carrying loss-of-function modifications at the target locus. This polyclonal format provides a robust, genetically diverse knockout model that avoids clonal selection biases and is suitable for a broad range of metabolic and cancer biology studies.
The AGS parental cell line originates from a human gastric adenocarcinoma and is widely used as a model of gastric mucosal epithelium. These cells form adherent monolayers that maintain key features of gastric epithelial barrier function and secretory capacity. AGS cells are particularly valued for investigating Helicobacter pylori infection mechanisms and gastric cancer pathogenesis, as they recapitulate the interaction between the pathogen and the host gastric epithelium over extended culture periods.
ECHS1 encodes mitochondrial short-chain enoyl-CoA hydratase, catalyzing the second step of mitochondrial fatty acid ??-oxidation: the reversible hydration of enoyl-CoA to 3-hydroxyacyl-CoA. This step is preferentially for short-chain substrates and is rate-limiting for the generation of acetyl-CoA and TCA cycle flux. ECHS1 expression is induced by PPAR??, HNF4??, and the co-activator PGC-1?? downstream of AMPK signaling. The ECHS1 protein forms homodimers and interacts with HADH and ACAA2 to form a functional ??-oxidation complex. Its disruption therefore blocks short-chain fatty acid catabolism and profoundly reduces mitochondrial energy output, affecting the entire pathway from SCAD (ACADS) and MCAD (ACADM) to the ETF/ETFDH electron transfer system.
In the AGS gastric cancer context, ECHS1 knockout models a critical metabolic vulnerability. Gastric cancer cells frequently reprogram energy metabolism, and mitochondrial fatty acid oxidation is an emerging target. Loss of ECHS1 in AGS cells compromises short-chain fatty acid oxidation, potentially reducing proliferation and survival under metabolic stress. This model also recapitulates aspects of human ECHS1 deficiency (Leigh syndrome, metabolic acidosis), allowing investigation of mitochondrial pathogenesis in an epithelial background. The polyclonal population preserves heterogeneity, making it ideal for studying metabolic adaptation and selection of subpopulations with altered mitochondrial function.
The ECHS1 Knockout AGS Polyclonal Cells enable a range of metabolic and cancer research applications. Typical assays include Seahorse mitochondrial respiration analysis, 14C-palmitate fatty acid oxidation assays, and acylcarnitine LC-MS profiling. Knockout confirmation and downstream pathway effects can be assessed by western blot (ECHS1, HADH, ACAA2) and RT-qPCR. Phenotypic assays such as MTT, annexin V apoptosis, and clonogenic survival reveal the impact on gastric epithelial cell viability. This model supports drug screening for mitochondrial disorders and gastric cancer metabolism, and can be used to study metabolic interactions during H. pylori infection. For further information or to discuss custom applications, please contact Ascent Research.
