The AXL Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from A-549 human lung adenocarcinoma cells, with targeted disruption of the AXL gene. This product provides a loss-of-function model for investigating AXL-dependent mechanisms in cancer biology. The polyclonal format maintains allelic heterogeneity, suitable for robust population-based assays without clonal bias.
The A-549 cell line, established from a 58-year-old male with lung carcinoma, is a widely used adherent epithelial model exhibiting alveolar type II characteristics. It recapitulates key features of non-small cell lung cancer (NSCLC), including EGFR signaling, EMT potential, and chemoresistance, making it an ideal host for AXL knockout studies.
AXL is a receptor tyrosine kinase activated primarily by GAS6, triggering downstream PI3K/AKT and MAPK/ERK pathways, along with JAK/STAT and NF-??B signaling. It interacts with coreceptors TYRO3 and MERTK, integrin ??1, and adaptors GRB2 and PI3K p85. AXL promotes expression of survival factors such as Bcl-2 and Survivin, EMT regulators SNAI1 and MMP9, and is itself upregulated by hypoxia, TGF-??, and EGFR ligands. This network drives cell proliferation, migration, and invasion.
In A-549 cells, AXL activation contributes to drug resistance and EMT. CRISPR/Cas9-mediated AXL disruption abolishes GAS6-induced phosphorylation of AKT and ERK1/2, attenuates STAT3 and NF-??B activity, and suppresses EMT markers. Consequently, these knockout cells show reduced proliferation, impaired migration, and enhanced apoptosis, providing a clean background to study AXL??s role in lung adenocarcinoma progression and therapy resistance.
Applications include western blotting for AXL, phospho-AKT (Ser473), and phospho-ERK1/2; RT-qPCR for downstream targets; cell proliferation (MTT/CCK-8) and apoptosis (Annexin V/PI) assays; Transwell migration/invasion experiments; and flow cytometry for surface AXL. The model supports AXL inhibitor screening, drug sensitivity testing with cisplatin or erlotinib, and phospho-signaling pathway analysis. For technical inquiries, contact Ascent Research.
