The ITGA6 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the A-549 human lung adenocarcinoma cell line, designed to disrupt ITGA6 gene function. This polyclonal pool contains a heterogeneous mix of cells with distinct editing events at the ITGA6 locus, providing a robust loss-of-function model that minimizes clonal selection artifacts. The product enables investigation of integrin ??6-dependent processes in a disease-relevant epithelial context without the bias introduced by single-cell cloning.
A-549 cells were originally established from explanted tumor tissue of a 58-year-old Caucasian male with lung adenocarcinoma and serve as a widely used in vitro model of human alveolar basal epithelial adenocarcinoma. These adherent, epithelial-like cells maintain key features of non-small cell lung cancer, including well-characterized growth factor signaling and ECM adhesion properties. Their genomic and transcriptomic stability makes them a suitable host for knocking out adhesion-related genes to study tumorigenic mechanisms.
ITGA6 encodes the integrin ??6 subunit, which heterodimerizes with ??1 (ITGB1) or ??4 (ITGB4) integrin to form laminin-binding receptors. These receptors interact with laminin subunits such as LAMA1, LAMB1, and LAMC1, and are modulated by intracellular adaptors including talin (TLN1) and kindlin-1 (FERMT1). Upon ligand engagement, ??6??1/??6??4 integrins recruit focal adhesion kinase (FAK/PTK2) and SRC kinase, initiating signaling through PI3K-AKT and MAPK1/3 (ERK2/1) cascades. Upstream, ITGA6 expression is regulated by transcription factors TP63, MYC, and TGFB1, and is influenced by the tumor suppressor TP53. Downstream effects include activation of AKT1, MAPK1/3, and BCL2, which collectively control cell survival, proliferation, and migration.
In A-549 lung adenocarcinoma cells, ITGA6-dependent adhesion to laminin contributes to anchorage-independent survival and invasive properties. Disruption of ITGA6 in this polyclonal knockout model impairs laminin binding and attenuates activation of PI3K/AKT and MAPK pathways, providing a platform to dissect integrin-driven mechanisms in tumor biology, epithelial-mesenchymal transition, and drug resistance. The polyclonal composition ensures that diverse loss-of-function mutations are represented, reducing artifacts in functional readouts.
These cells are tailored for a variety of experimental applications, including western blotting to confirm ITGA6 protein loss, RT-qPCR to assess mRNA levels, flow cytometry for surface integrin profiling, cell adhesion assays on laminin-coated substrates, Boyden chamber migration and invasion assays, anoikis resistance testing, and phospho-signaling analysis (e.g., phospho-FAK, phospho-AKT). They are valuable for studying integrin ??6 biology in lung cancer, validating anti-integrin therapeutic candidates, and exploring mechanisms of metastatic progression. For technical support, detailed protocols, or ordering information, please contact Ascent Research.
