The CD3E Knockout A2780 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout population derived from the human A2780 ovarian carcinoma cell line. This targeted disruption of the CD3E gene abrogates expression of the CD3 epsilon chain, a core component of the T-cell receptor (TCR) complex. As a non-clonal, heterogeneous cell pool, the model reflects diverse CRISPR/Cas9 editing outcomes, eliminating CD3E-mediated signaling and providing a clean background for studying TCR-independent functions or serving as a stringent negative control in T-cell activation assays.
The parental A2780 cell line is an extensively characterized epithelial ovarian carcinoma model, originally isolated from an untreated patient. These cells grow as an adherent monolayer and are widely employed in ovarian cancer research for investigations into drug resistance, metastasis, and tumorigenicity via xenograft models. The availability of a CD3E-knockout derivative on this established platform enables controlled studies of ovarian cancer biology in the absence of potential CD3E influences.
CD3E encodes the CD3 epsilon subunit, which assembles with CD3??, CD3??, CD3??, and TCR???? to form the TCR-CD3 complex. Antigen-MHC engagement triggers Lck- and Fyn-mediated phosphorylation of CD3 ITAMs, thereby recruiting and activating ZAP70. ZAP70 subsequently phosphorylates adaptors LAT and SLP-76, initiating a signaling cascade that recruits PLC??1, GRB2, and other effectors. This leads to Ca2? mobilization, PKC??-driven CARMA1/BCL10/MALT1 complex formation, and NF-??B activation. Concurrently, MAPK pathways (ERK, JNK, p38) and PI3K-Akt signaling are stimulated. Thus, CD3E functions as a critical proximal transducer coupling TCR engagement to transcriptional reprogramming in T cells.
In A2780 cells, CD3E is not endogenously expressed at significant levels; targeted removal of the gene eradicates any residual or experimentally introduced expression that could confound results. This knockout model is particularly valuable for ovarian cancer studies examining immune privilege, as it permits dissection of potential non-canonical CD3E functions in epithelial tumors. It also provides an essential negative control for bispecific antibody therapies and CAR-T cell experiments, ensuring that observed cytotoxic effects are T-cell?Cspecific. The polyclonal nature of the population reduces clonal artifacts and preserves the epithelial ovarian carcinoma background.
This polyclonal knockout model supports diverse applications, including validation of CD3E as a therapeutic target in cancer immunotherapy, screening of TCR pathway inhibitors, and functional reconstitution assays. Standard characterization methods include Western blotting, RT-qPCR, immunofluorescence, and flow cytometry to confirm CD3E ablation. Co-immunoprecipitation can delineate altered protein interaction networks, while cell viability and drug sensitivity assays assess therapeutic responses. Additionally, these cells enable xenograft studies dissecting tumor-immune interactions. For technical details or purchasing information, please contact Ascent Research.
