The CD3E Knockout AGS Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population from the AGS human gastric adenocarcinoma line, with CD3E gene disruption. This loss-of-function model provides a genetically defined system for investigating CD3E-mediated signaling in gastric cancer. The polyclonal population preserves tumor cell heterogeneity, avoiding clonal selection biases.
The AGS cell line is an epithelial model established from a primary gastric adenocarcinoma of a female patient, widely used for gastric cancer research. It recapitulates key tumor biology aspects such as proliferation, migration, and drug response, serving as a platform for studying molecular mechanisms and preclinical therapy evaluation.
CD3E encodes the CD3 epsilon chain, an essential subunit of the T-cell receptor/CD3 complex required for TCR assembly, signal transduction, and T-cell development. Although primarily characterized in T lymphocytes, CD3E expression has been noted in certain cancers. In the TCR signaling cascade, CD3E interacts with CD3??, CD3??, and CD3?? to form the CD3 complex with TCR??/??. Upon receptor engagement, CD3E is phosphorylated by Src family kinases LCK and FYN, subsequently recruiting and activating ZAP70, which then phosphorylates LAT and SLP-76, leading to PLC??1 activation and downstream signaling through calcium and MAPK pathways. This culminates in the activation of transcription factors NFAT, NF-??B, and AP-1.
In the AGS context, CD3E knockout eliminates CD3E-mediated signaling, enabling dissection of non-immune CD3E functions potentially contributing to tumor behavior. This model is valuable for exploring crosstalk between gastric adenocarcinoma signaling networks and CD3E-dependent pathways, and for examining tumor?Cmicroenvironment interactions. The knockout allows study of effects on proliferation, survival, migration, and invasion without clonal adaptation artifacts.
Research applications include functional characterization of CD3E in gastric cancer, non-canonical signaling investigation, tumor immunology studies, drug target validation, and xenograft modeling. Compatible assays comprise western blotting, RT-qPCR, immunofluorescence, flow cytometry, proliferation, apoptosis, migration/invasion, colony formation, and xenograft tumor growth. For additional information, contact Ascent Research.
