The EFNA5 Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, with disruption of the EFNA5 gene. This heterogeneous pool of cells provides a loss-of-function model to study ephrin-A5 biology in an epithelial ovarian cancer background without clonal biases. The polyclonal format is ideal for assessing EFNA5-dependent phenotypes at the population level and for investigating receptor-ligand interactions and cytoskeletal regulation.
The A2780 cell line originates from an untreated patient with ovarian endometrioid adenocarcinoma and is a well-established model of epithelial ovarian cancer. These adherent cells retain key oncogenic pathways and are extensively used in studies of tumor progression, drug response, and metastasis. Employing A2780 as the host line enables direct functional analysis of EFNA5 in a clinically relevant ovarian cancer context.
EFNA5 encodes ephrin-A5, a GPI-anchored ligand that binds Eph receptor tyrosine kinases such as EPHA3, EPHA4, EPHA7, and EPHB2, triggering bidirectional signaling. Ephrin-A5 reverse signaling and Eph forward signaling converge on small GTPases RHOA, RAC1, and CDC42, and downstream effectors including ERK and AKT, to regulate cytoskeletal dynamics and adhesion. The ephrin-A5/EPHA4 pathway activates the RHOA-ROCK-LIMK-cofilin cascade, promoting actin polymerization and cell repulsion. Upstream, EFNA5 is transcriptionally regulated by TP53, WNT/??-catenin, and Notch, linking ephrin signaling to key tumor-modifying networks.
In A2780 ovarian carcinoma cells, disruption of EFNA5 impairs ephrin-Eph repulsive signaling, which can diminish cell-cell repulsion and enhance migratory and invasive behavior??phenotypes associated with ovarian cancer metastasis. This knockout model allows researchers to dissect how ephrin-A5 loss influences tumor-stroma interactions, anoikis resistance, and chemosensitivity. By eliminating ephrin-A5, both forward and reverse signaling contributions to epithelial homeostasis and invasiveness can be examined.
This polyclonal knockout product supports diverse functional assays, including wound healing and transwell migration/invasion assays to quantify motility changes. Molecular readouts may include western blotting for phospho-Eph receptors, phospho-ERK, and phospho-AKT, as well as immunofluorescence for focal adhesion markers. RT-qPCR profiling of ephrin target genes and flow cytometry for adhesion molecules complement the phenotypic analysis. The model is also valuable for investigating drug resistance and cross-talk with oncogenic pathways. For further information, please contact Ascent Research.
