The EFNA1 Knockout AGS Polyclonal Cells product is a pool of CRISPR/Cas9-edited AGS gastric adenocarcinoma cells engineered for disruption of the EFNA1 gene. This heterogeneous polyclonal knockout cell population provides a flexible loss-of-function model without requiring single-cell clonal isolation, enabling researchers to study ephrin-A1-dependent signaling in a human gastric epithelial context.
The AGS cell line originates from a patient with gastric adenocarcinoma and serves as a well-established in vitro model of gastric cancer. As epithelial tumor cells, AGS retain relevant receptor tyrosine kinase expression and downstream signaling machineries that drive proliferation, migration, and invasion, making them a suitable host for interrogating oncogenic pathways.
EFNA1 encodes ephrin-A1, a GPI-anchored ligand that binds EphA2 and EphA4 receptors, activating bidirectional signaling. Key mediators include SRC, FAK, and adaptor GRB4, leading to MAPK/ERK cascade activation via GRB2?CSOS?CRAS?CRAF1?CMAP2K1?CMAPK1 and PI3K/AKT pathway stimulation through PIK3CA?CAKT1. Ephrin-A1/EphA signaling also modulates Rho GTPases (RAC1, RHOA) and effectors ROCK1 and ACTR2/3, controlling actin cytoskeleton dynamics. Upstream, EFNA1 expression is influenced by TNF-??, IL-1??, HIF-1??, and transcription factors p53 and NF-??B, linking extracellular signals to cellular responses.
In AGS cells, EFNA1 disruption abolishes ephrin-A1/EphA forward and reverse signaling, attenuating SRC and FAK activity and reducing MAPK/ERK and PI3K/AKT pathway output. Consequently, Rho GTPase-driven actin remodeling, cell migration, and invasion are impaired. Downregulation of MMP9 further diminishes invasive potential, highlighting the model??s relevance for dissecting EFNA1??s role in gastric cancer aggressiveness within a heterogeneous cell population.
Researchers can employ this polyclonal knockout pool to investigate EFNA1-dependent modulation of EphA2 phosphorylation, cell migration (wound healing, Transwell invasion), proliferation (MTT assay), apoptosis (flow cytometry), and F-actin organization (immunofluorescence). Western blotting and RT-qPCR enable analysis of pathway components such as phospho-ERK, AKT, and MMP9. The model also supports drug screening for EphA receptor inhibitors and tumor microenvironment studies. For further details, contact Ascent Research.
