The EFNB3 Knockout A2780 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, featuring targeted disruption of the EFNB3 gene. This polyclonal knockout model provides a genetically heterogeneous pool of cells lacking functional ephrin B3, enabling robust loss-of-function studies without clonal biases. CRISPR/Cas9-mediated gene disruption abrogates ephrin B3-mediated signaling, allowing dissection of EFNB3 contributions in an ovarian cancer context.
A2780 is an epithelial ovarian carcinoma cell line established from an untreated patient, widely used for drug resistance and metastasis research. Exhibiting epithelial morphology and retaining key signaling pathways of high-grade serous ovarian cancer, A2780 is an ideal host for studying ephrin B3 in migration, invasion, and adhesion. Its established response to chemotherapeutics and xenograft tumorigenicity further supports translational applications.
Ephrin B3 (EFNB3) functions as a transmembrane ligand for EphB receptors (EphB1, EphB2), mediating contact-dependent bidirectional signaling. Forward signaling activates Src family kinases, Rho GTPases (Rac, RhoA), and FAK, engaging MAPK/ERK and PI3K/AKT pathways. Reverse signaling recruits PDZ-domain proteins such as GRIP1 and syndecan, regulating cytoskeletal dynamics and integrin adhesion. EFNB3 is controlled by hypoxia (HIF1??), Notch, and FGF signals, and it participates in axon guidance, boundary formation, and angiogenesis. In cancer, its EphB interactions drive cell repulsion and migration.
In A2780 cells, EFNB3 knockout disrupts Eph/ephrin bidirectional signaling, impairing Rho GTPase-mediated cytoskeletal reorganization and FAK-dependent adhesion. This polyclonal knockout model likely reduces ephrin B3-driven migration and invasion, attenuating metastatic potential while avoiding clonal artefacts. Loss of EFNB3 may also alter MAPK/ERK and PI3K/AKT pathway activity, providing a tool to examine signaling crosstalk and resistance mechanisms in ovarian cancer progression.
Key applications include transwell migration and invasion assays, immunofluorescence for actin dynamics, Western blotting for phosphorylated ERK and FAK, and co-immunoprecipitation to assess EphB receptor interactions. RNA-seq enables transcriptomic analysis of pathway changes. The model is suited for drug screening targeting the ephrin/Eph axis and tumor microenvironment studies. For further details, please contact Ascent Research.
