The CD320 Knockout AGS Polyclonal Cells are a ready-to-use, CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line. This product provides a heterogeneous pool of cells carrying targeted disruptions in the CD320 gene, enabling loss-of-function studies of the transcobalamin receptor in a gastric cancer context. The knockout model is generated without single-cell cloning, preserving a polyclonal background suitable for bulk population analyses.
AGS is a widely employed model of gastric epithelial adenocarcinoma, originally established from a primary tumor of a 54-year-old female. These adherent epithelial cells retain key characteristics of gastric adenocarcinoma and are extensively used in cancer biology research, including investigations of tumorigenesis, signaling, and drug response. Their relevance to gastric pathology makes them a valuable platform for examining cobalamin-related metabolic pathways and epigenetic regulation.
CD320 encodes the high-affinity receptor for transcobalamin II (TCN2) saturated with cobalamin (vitamin B12). Upon binding the circulating TCN2-cobalamin complex, CD320 mediates endocytic uptake of the micronutrient, which serves as an essential cofactor for two cytoplasmic enzymes: methionine synthase (MTR) and methylmalonyl-CoA mutase (MUT). Consequently, CD320 function is pivotal for homocysteine remethylation to methionine, the subsequent generation of the universal methyl donor S-adenosylmethionine (SAM), and the conversion of methylmalonyl-CoA to succinyl-CoA. CD320 activity is therefore situated upstream of MTR, MUT, homocysteine, methylmalonyl-CoA, and SAM. Regulatory inputs include the abundance of the TCN2-cobalamin complex and cellular methylation demand, while the receptor is known to interact with TCN2 and with the multiligand receptor LRP2.
In the AGS gastric adenocarcinoma setting, disruption of CD320-mediated cobalamin import is anticipated to compromise one-carbon metabolism and the methylation cycle, leading to altered homocysteine and methylmalonic acid levels and perturbed DNA methylation profiles. Such metabolic stress can influence cell proliferation, apoptosis, and epigenetic plasticity, making the knockout cells particularly informative for studying links between vitamin B12 status and gastric cancer progression. The model also provides a relevant tool for investigating conditions associated with cobalamin insufficiency, such as megaloblastic anemia and methylmalonic aciduria.
These polyclonal knockout cells are suited to a broad range of functional assays, including cobalamin uptake experiments, homocysteine ELISA, methylmalonic acid quantification, cell proliferation (MTS) and apoptosis analyses, and DNA methylation profiling. They also enable mechanistic dissection of TCN2/cobalamin-dependent signaling and drug sensitivity screens targeting methylation-dependent pathways. For ordering, licensing, or technical inquiries, please contact Ascent Research.
