The ECI1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma cell line, featuring targeted disruption of the ECI1 gene. This loss-of-function model eliminates mitochondrial enoyl-CoA delta isomerase 1 activity, enabling precise investigation of unsaturated fatty acid ??-oxidation in a gastric cancer context. The polyclonal format retains population heterogeneity, ensuring robust gene disruption and making it ideal for metabolic studies requiring bulk cellular responses while minimizing clonal selection artifacts.
HGC-27 is a widely characterized poorly differentiated gastric adenocarcinoma cell line originally isolated from a lymph node metastasis. It retains hallmark features of aggressive gastric cancer, including mucin production, high proliferative capacity, and metabolic adaptability. As a metastatic gastric cancer model, HGC-27 provides a clinically relevant system for probing metabolic reprogramming mechanisms that sustain tumor growth under nutrient-deprived conditions. The poorly differentiated phenotype reflects advanced disease stages, facilitating the study of metabolic vulnerabilities in lethal malignancies.
ECI1 encodes a mitochondrial enzyme that catalyzes the isomerization of 3-cis-enoyl-CoA to 2-trans-enoyl-CoA, an essential reaction in ??-oxidation of unsaturated fatty acids. ECI1 operates downstream of nutrient-sensing pathways, transcriptionally regulated by PPARA and PPARGC1A, and modulated by AMPK and SIRT1. It physically interacts with HADHA, HADHB, and ECHS1, forming a functional unit within the fatty acid degradation pathway that also includes CPT1A, CPT2, ACADM, ACADVL, and ACAA1. The isomerization step is required for subsequent hydration and thiolytic cleavage, producing acetyl-CoA, NADH, and FADH2 to fuel the TCA cycle and oxidative phosphorylation. Thus, ECI1 integrates hormonal and energy signals to control mitochondrial ATP output; its disruption reroutes lipid flux and impairs energy homeostasis.
In HGC-27 gastric cancer cells, loss of ECI1 severely compromises unsaturated fatty acid utilization, imposing metabolic stress and potentially revealing targetable liabilities. Many cancers, especially metastatic phenotypes, depend on fatty acid oxidation for proliferation and survival; this knockout model dissects the specific contribution of unsaturated fatty acid catabolism to gastric cancer pathophysiology. It is valuable for investigating how metabolic reprogramming supports poorly differentiated adenocarcinoma, where abnormal lipid metabolism is a hallmark. Eliminating ECI1 allows assessment of cell viability, apoptosis, and metabolic adaptation.
These polyclonal knockout cells support diverse applications, including [U-13C]palmitate metabolic flux assays, Seahorse mitochondrial stress tests, and ATP luminescence measurements. They facilitate drug target validation, synthetic lethality screening, and exploration of metabolic vulnerabilities in gastric cancer. Validation can be performed by Western blotting, RT-qPCR, and phenotypic assays such as proliferation, apoptosis, and metabolomics profiling. The polyclonal format avoids clonal artifacts, improving biological relevance. For further details or custom requests, please contact Ascent Research.
