The ITGA2 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the A-549 human lung adenocarcinoma cell line, featuring disruption of the ITGA2 gene. This heterogeneous pool lacks functional integrin alpha-2, providing a robust loss-of-function model for studying integrin-mediated cell adhesion and signaling without clonal selection.
The A-549 cell line serves as a model of human alveolar basal epithelial cells, retaining characteristics of type II pneumocytes. Widely used in cancer research, A-549 cells are ideal for investigating lung adenocarcinoma metastasis, epithelial barrier function, and therapeutic responses, making them a suitable host for CRISPR/Cas9-mediated gene disruption.
ITGA2 encodes integrin alpha-2, which heterodimerizes with ITGB1 to form a collagen/laminin receptor. Ligand binding activates FAK and Src kinase, leading to paxillin phosphorylation and signaling through the small GTPases Rac1 and RhoA, modulating cytoskeletal dynamics via RhoA/ROCK. This pathway also stimulates PI3K-AKT survival signaling and Erk1/2 proliferation. Upstream, ITGA2 expression is regulated by SP1, TGF-??1, TNF-??, ECM stiffness, and miR-128. Key interactors include talin, kindlin, and CD151, which stabilize adhesion complexes, and downstream, MMP expression is induced.
In A-549 cells, ITGA2-mediated adhesion to collagen is critical for migration and invasion. Knockout of ITGA2 impairs collagen attachment and directed migration, providing a relevant model for studying lung cancer metastasis and tumor invasiveness. The polyclonal nature reduces clonal artifacts and reflects tumor heterogeneity, making it suitable for drug screening targeting integrin pathways.
These knockout cells are applicable in collagen adhesion assays, scratch wound healing, transwell migration/invasion, and immunofluorescence of focal adhesions. Western blot for phospho-FAK, flow cytometry for integrin alpha-2, RNA-seq, and cell viability assays under drug treatment can be performed. They support screening for integrin inhibitors and epithelial barrier studies. For inquiries, contact Ascent Research.
