The ITGA3 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 ITGA3 gene. This loss-of-function model allows researchers to investigate integrin alpha-3 biology in an epithelial context. The polyclonal format provides a heterogeneous pool of edited cells, suitable for population-based functional studies.
The A-549 host cell line originates from a 58-year-old male and harbors a KRAS G12S mutation. As a widely used alveolar epithelial model, it is employed in cancer biology, drug discovery, and pulmonary disease research, offering a well-characterized genetic and phenotypic background for knockout screening.
ITGA3 encodes the integrin alpha-3 subunit, which forms a heterodimer with integrin beta-1 (ITGB1) to bind laminin, collagen, and fibronectin. This interaction triggers focal adhesion kinase (FAK) and Src activation, leading to PI3K/Akt and MAPK/ERK pathway stimulation. Upstream regulators such as TGF-beta, EGF, and HGF modulate ITGA3 expression, while downstream FAK/Src signals influence Rho GTPases (RhoA, Rac1), matrix metalloproteinases (MMPs), and transcription factors SP1 and AP-1. These pathways coordinate cell adhesion, migration, and epithelial-mesenchymal transition (EMT). The integrin complex also interacts with talin, vinculin, paxillin, and tetraspanins, thereby linking ECM engagement to cytoskeletal reorganization and intracellular signaling cascades.
In the A-549 lung adenocarcinoma background, ITGA3 contributes to adhesion-dependent proliferation and migration. Knockout of ITGA3 disrupts integrin-mediated ECM sensing, likely impairing FAK autophosphorylation, Akt and ERK activation, and the expression of EMT-associated markers. This model enables dissection of integrin crosstalk with oncogenic KRAS signaling, providing insights into how adhesion signaling modulates tumor cell plasticity, invasive potential, and drug response in a genetically defined lung cancer context.
These polyclonal knockout cells are ideal for cell adhesion assays on ECM substrates, wound healing and Boyden chamber invasion assays, and quantitative phospho-signaling analysis (pFAK, pAkt, pERK). They can also be employed in immunofluorescence to visualize focal adhesion dynamics, RNA-seq for transcriptome-wide effects of ITGA3 loss, and flow cytometry to assess surface integrin levels. This model serves as a robust platform for investigating integrin signaling in cancer metastasis, pulmonary fibrosis, and adhesive drug resistance mechanisms. For additional information, please contact Ascent Research.
