The EED Knockout AGS Polyclonal Cells product comprises a polyclonal population of AGS human gastric adenocarcinoma cells edited using CRISPR/Cas9 to disrupt the endogenous EED gene. This polyclonal knockout pool offers a versatile loss-of-function model for interrogating the Polycomb Repressive Complex 2 (PRC2) pathway without clonal selection artifacts. The heterogeneous cell population retains the diverse genetic background of the parental line while uniformly carrying targeted disruptions at the EED locus, enabling robust functional studies of epigenetic regulation in a gastric cancer context.
AGS cells are an established adherent human gastric adenocarcinoma epithelial cell line widely employed in gastric cancer research. Derived from a primary adenocarcinoma, AGS cells display epithelial morphology and key features of gastric tumorigenesis, including aberrant signaling pathways and tumor suppressor silencing. Their well-characterized molecular landscape makes them a suitable host for evaluating the consequences of epigenetic modifier loss in a disease-relevant in vitro system.
EED encodes an essential subunit of PRC2 that selectively binds trimethylated histone H3 lysine 27 (H3K27me3) and allosterically stimulates the methyltransferase activity of EZH2. Through this positive feedback mechanism, EED facilitates the propagation of H3K27me3 marks across chromatin, leading to stable transcriptional repression of target genes including HOX clusters, CDKN2A (p16INK4a), and CDKN1A (p21). EED functions within a core complex containing EZH2, SUZ12, and RBBP4/7, and its activity is modulated by upstream signals such as AKT, CDK1, and MYC. Disruption of EED therefore abolishes PRC2 catalytic activity, resulting in global loss of H3K27me3 and de-repression of critical tumor suppressors and developmental regulators.
In the AGS gastric adenocarcinoma model, EED knockout has profound biological consequences: PRC2-dependent silencing is dismantled, leading to reactivation of pro-apoptotic and cell cycle inhibitory genes like CDKN2A and PTEN, and attenuation of oncogenic transcriptional programs. This system models the therapeutic effects of EZH2/EED inhibitors, as PRC2 loss mimics pharmacological disruption. Consequently, these polyclonal knockout cells serve as a powerful tool for dissecting PRC2 functional dependencies in gastric cancer, assessing epigenetic drug sensitivity, and identifying novel downstream effectors that restrain tumor cell growth.
Researchers can utilize EED Knockout AGS Polyclonal Cells in a broad array of applications, including profiling transcriptomic and epigenomic changes by RNA-seq and ChIP-seq, quantifying H3K27me3 and PRC2 component levels via western blotting or mass spectrometry, and evaluating tumor suppressor re-expression by RT-qPCR. Cellular phenotypic assays such as MTT viability, colony formation, and Annexin V apoptosis measurements enable direct assessment of growth inhibition and cell death. Additionally, these cells are ideal for testing the efficacy and specificity of EZH2 or EED inhibitors in a PRC2-disrupted background. For ordering details and technical support, please contact Ascent Research.
