The EDC3 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the AGS human gastric adenocarcinoma cell line. This product provides a loss-of-function model for EDC3, a key enhancer of mRNA decapping, enabling studies of post-transcriptional regulation and processing body (P-body) dynamics without clonal selection bias.
The AGS host cells are an adherent epithelial line derived from a female gastric adenocarcinoma patient. Widely employed to investigate gastric carcinogenesis and Helicobacter pylori infection, AGS cells offer a well-characterized transcriptomic and proteomic background for functional genomics. Their relevance to human gastric cancer makes them an ideal host for targeted disruption of genes involved in RNA metabolism.
EDC3 is a scaffold protein that localizes to P-bodies and potentiates the decapping activity of DCP2, thereby channeling mRNAs into the 5??-to-3?? exonucleolytic pathway mediated by XRN1. It interacts with DCP1A, DDX6, EDC4, PATL1, LSM14A, and the CNOT1 subunit of the CCR4?CNOT complex. P-body assembly and EDC3 function are influenced by stress granule dynamics, mTOR signaling, and miRNA-mediated silencing. Consequently, loss of EDC3 can stabilize mRNAs encoding regulators of proliferation, stress adaptation, and oncogenic signaling, providing a tool to dissect the post-transcriptional layer of gastric cancer biology.
In the AGS background, EDC3 knockout allows dissection of how altered mRNA decay impacts gastric cancer phenotypes, including epithelial-mesenchymal transition, invasion, and drug responsiveness. Because gastric adenocarcinomas frequently exhibit dysregulated RNA decay, this polyclonal knockout pool supports high-content screening and averaging of clonal variability while ensuring robust target-gene disruption at the population level.
This model is compatible with diverse downstream analyses: RT-qPCR for mRNA half-life determination, RNA-seq for transcriptome-wide profiling, immunofluorescence for P-body visualization, and co-immunoprecipitation of decapping complex components such as DCP1A and DCP2. Phenotypic assays??including migration and invasion tests, MTT-based drug sensitivity profiling, and phospho-signaling arrays??can further link EDC3 loss to functional outcomes. For additional information, please contact Ascent Research.
