The ECI2 Knockout HGC-27 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line, featuring targeted disruption of the ECI2 gene. This loss-of-function model enables investigation of peroxisomal enoyl-CoA delta isomerase function in a gastric cancer background. The polyclonal format provides a heterogeneous pool of edited cells for robust functional studies.
HGC-27 cells were established from a lymph node metastasis of a gastric adenocarcinoma in a 63-year-old male, providing a model for metastatic gastric epithelial carcinoma. This cell line retains oncogenic features and altered metabolism, making it suitable for studying lipid metabolism in gastric cancer progression.
ECI2 encodes a peroxisomal enoyl-CoA delta isomerase that catalyzes the isomerization of 3-cis and 3-trans unsaturated fatty acyl-CoA intermediates to 2-trans isomers, a crucial step in peroxisomal ??-oxidation of polyunsaturated fatty acids. The enzyme interacts with PEX5 for peroxisomal import and functions in concert with ACOX1, D-bifunctional protein, and 3-ketoacyl-CoA thiolase within the core ??-oxidation complex. Transcriptional regulation is mediated by PPAR?? and PPAR?? in response to fatty acid ligands. Knockout impairs this conversion, leading to accumulation of metabolic intermediates and reduced generation of acetyl-CoA, NADH, and FADH2, thereby altering cellular energy metabolism.
In gastric adenocarcinoma, metabolic reprogramming is a hallmark of malignant transformation, with cancer cells frequently exhibiting altered lipid utilization to support proliferation. The ECI2 knockout HGC-27 model allows dissection of peroxisomal unsaturated fatty acid oxidation’s contribution to the gastric cancer metabolic phenotype. Abrogating ECI2 disrupts the peroxisomal ??-oxidation arm, potentially sensitizing cells to lipid stress and uncovering metabolic vulnerabilities linked to energy provision, redox balance, or signaling lipid production.
Applications include fatty acid oxidation assays, lipidomic profiling, peroxisomal ??-oxidation activity measurements, and metabolic flux analysis using labeled substrates. Validation of ECI2 disruption can be performed via RT-qPCR and Western blotting, while functional studies employ ATP production assays, cell proliferation tests, and immunofluorescence for peroxisomal markers. The model supports co-culture or spheroid experiments to assess peroxisomal lipid metabolism in tumor microenvironment contexts, and drug screening for synthetic lethal interactions. For further information, contact Ascent Research.
