The ANTXR1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line, designed for targeted disruption of the ANTXR1 gene. ANTXR1 encodes a type I transmembrane protein that functions in cell adhesion and angiogenesis and serves as the receptor for anthrax protective antigen. The polyclonal format provides a heterogeneous pool of knockout cells, minimizing clonal selection bias while preserving population-level diversity essential for robust functional assays. Loss of ANTXR1 protein expression can be confirmed by western blotting, enabling direct assessment of the molecular consequences of ANTXR1 depletion.
The A-549 host cell line was established from a 58-year-old Caucasian male with lung adenocarcinoma and serves as a well-characterized model of alveolar basal epithelial cells. This cell line is extensively employed in non-small cell lung cancer research, anthrax toxin studies, and investigations of cell?Cmatrix interactions. Its expression of key integrins and extracellular matrix receptors creates an ideal background for exploring ANTXR1-dependent processes such as adhesion, migration, and angiogenesis in a tumor-relevant setting.
ANTXR1 interacts with collagen type I, collagen type IV, and laminin via integrin beta1 engagements, triggering activation of focal adhesion kinase (FAK), SRC, AKT1, and the MAPK1/3 (ERK1/2) cascade. This signaling axis promotes endothelial cell migration and angiogenesis. ANTXR1 also mediates anthrax protective antigen (PA)-dependent toxin internalization. Expression of ANTXR1 is regulated by hypoxic conditions and pro-angiogenic factors including VEGF, FGF2, and the transcription factor HIF1A, positioning ANTXR1 as a critical effector downstream of angiogenic and hypoxic stimuli.
In A-549 adenocarcinoma cells, ANTXR1 knockout disrupts focal adhesion signaling and attenuates AKT and MAPK pathway activation, thereby impairing cell adhesion, migration, and invasive capacity. The polyclonal knockout population mirrors tumor heterogeneity and reduces artifacts associated with clonal selection, making it suitable for wound healing and Matrigel invasion assays. This model enables precise dissection of ANTXR1’s contribution to lung carcinoma progression and evaluation of its potential as an anti-angiogenic therapeutic target.
Applications include investigating tumor angiogenesis mechanisms, assessing anthrax toxin susceptibility, studying cell?Cmatrix adhesion, and validating anti-angiogenic drug candidates. Researchers can perform western blotting for knockout confirmation, cell adhesion and wound healing assays, Matrigel invasion, phospho-FAK and phospho-AKT analysis, anthrax toxin sensitivity testing, and transcriptome profiling by RNA-seq. For validation data, protocols, or customization inquiries, contact Ascent Research.
