The EFNB3 Knockout AGS Polyclonal Cells represent a powerful CRISPR/Cas9-edited polyclonal knockout cell population designed for studying EFNB3 gene function in a human gastric epithelial context. This polyclonal knockout model disrupts the expression of ephrin-B3, a transmembrane ligand critical for Eph receptor-mediated bidirectional signaling, offering a loss-of-function platform to investigate the role of ephrin-B3 in gastric cancer cell biology. The use of a polyclonal population captures the heterogeneity of gene editing outcomes, providing a robust tool for functional studies without the bias of single-cell cloning.
The host AGS cell line is derived from a human gastric adenocarcinoma and serves as a well-established model for gastric cancer research. These adherent epithelial cells retain key characteristics of gastric tumor cells, making them suitable for investigating oncogenic signaling, cell adhesion, and metastatic processes. The AGS background is widely used to explore molecular mechanisms underlying gastric adenocarcinoma progression and to screen potential therapeutic interventions.
Ephrin-B3, encoded by EFNB3, functions as a transmembrane ligand for Eph receptors, primarily EphA4 and EphB2, initiating bidirectional signaling upon cell-cell contact. This signaling controls cytoskeletal dynamics and cell motility by modulating downstream targets such as RhoA, ROCK, FAK, and Akt, and integrin activation. Ephrin-B3 also interacts with PDZ domain proteins and SH2/SH3 adaptor proteins, integrating FGF signals. Disruption of ephrin-B3 uncouples these cascades, allowing dissection of Eph/ephrin communication in cell migration and tissue organization.
In the AGS gastric cancer model, knockout of ephrin-B3 is expected to impair cell migration, invasion, and proliferation due to the perturbation of Rho GTPase and integrin signaling networks. This loss-of-function model allows researchers to examine how ephrin-B3-mediated signaling influences gastric tumor cell behavior, including epithelial-mesenchymal transition and metastatic dissemination. By eliminating ephrin-B3 function, the cells become a valuable tool for elucidating the molecular dependencies of gastric adenocarcinoma on Eph/ephrin circuitry.
These polyclonal knockout cells are ideal for a range of experimental applications, including transwell migration and invasion assays, proliferation analyses via MTT or BrdU incorporation, and signaling studies through western blotting or RT-qPCR to quantify key pathway components like FAK, Akt, and RhoA. Flow cytometry can be used to profile surface expression changes in adhesion molecules or integrins. Moreover, the cells enable high-content screening for compounds targeting Eph/ephrin signaling in gastric cancer. For further technical details and ordering information, please contact Ascent Research.
