The EFNA5 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma epithelial cell line. This product facilitates loss-of-function analysis by disrupting the EFNA5 gene, which encodes the ephrin-A5 ligand. The polyclonal nature of the population ensures a heterogeneous mix of knockout cells, providing a robust and reproducible model for functional studies without the clonal biases of single-cell isolates.
The A-549 cell line was established from the lung adenocarcinoma of a 58-year-old Caucasian male and serves as a widely used model for non-small cell lung cancer and epithelial barrier research. These adherent cells retain characteristics of alveolar type II pneumocytes and harbor key genetic alterations, including mutations in KRAS and TP53, which mirror clinically relevant oncogenic backgrounds. This makes A-549 an ideal host for investigating tumor cell biology, drug responses, and metastatic mechanisms.
Ephrin-A5, the product of EFNA5, is a glycosylphosphatidylinositol (GPI)-anchored ligand that binds to EphA receptor tyrosine kinases (EphA1?C5) to initiate bidirectional signaling. This interaction regulates cell adhesion, repulsion, and migration through downstream effectors such as SRC family kinases, focal adhesion kinase (FAK), and Rho GTPases, ultimately feeding into the PI3K-Akt and MAPK signaling cascades. Ephrin-A5 activity is modulated by upstream regulators including p53 family members, TGF-??, Wnt, and HIF-1??, and involves interactions with lipid raft microdomains and ADAM metalloproteases that mediate ligand shedding.
In the context of lung adenocarcinoma, ephrin-A5 has been implicated in promoting tumor progression, angiogenesis, and metastasis. Dysregulated ephrin-Eph signaling can enhance invasive phenotypes and contribute to resistance against conventional therapies. By ablating EFNA5 in A-549 cells, this knockout model enables researchers to dissect the specific contributions of ephrin-A5 to cancer cell motility, proliferation, and survival, particularly in the presence of driving mutations such as KRAS.
Typical research applications include Western blotting and RT-qPCR for confirmation of gene disruption, wound healing and Transwell invasion assays to evaluate migratory and invasive capacity, and proliferation or apoptosis detection kits for functional studies. Phospho-signaling arrays can map altered kinase networks in the absence of ephrin-A5, while tumor xenograft models permit in vivo assessment of EFNA5??s role in tumor growth and drug response. For further information or custom inquiries, please contact Ascent Research.
