CD44 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell pool derived from the A-549 human lung adenocarcinoma line. Through targeted disruption of the CD44 gene, this product provides a functional loss-of-function model for studying the hyaluronan receptor CD44, a transmembrane glycoprotein implicated in cell adhesion, migration, and oncogenic signaling. The polyclonal format ensures a heterogeneous population of cells carrying diverse mutations at the CD44 locus, minimizing clonal artifacts and offering a broad representation of knockout phenotypes. This CRISPR/Cas9-mediated gene disruption abrogates CD44-mediated signaling, enabling researchers to dissect its roles in cancer biology without the bias of single-cell selection.
The parental A-549 cell line originates from a human lung adenocarcinoma and exhibits an epithelial morphology with a hypotriploid karyotype. Widely employed as a model for alveolar epithelial cells, A-549 cells retain features of type II pneumocytes and are extensively used in studies of lung cancer, metastasis, and drug resistance. Their robust growth characteristics and well-characterized signaling landscape make them an ideal host for investigating the molecular mechanisms of CD44 in a clinically relevant adenocarcinoma context.
CD44 functions as a receptor for hyaluronan and osteopontin, mediating cell adhesion and signaling. Ligand binding triggers CD44 interaction with ERM proteins and ankyrin, activating Src kinases that propagate signals through PI3K/AKT and MAPK/ERK cascades. Key intermediates include RAS, MEK, ERK, and Rho GTPases (Rac1, Cdc42), which phosphorylate cortactin and paxillin, and upregulate MMP9. Downstream transcription factors such as ??-catenin, SNAI1, and TWIST1 drive EMT. CD44 expression is induced by WNT ligands, TGF-??, and hypoxia via NF-??B, and it functionally interacts with CD74 and EGFR.
In A-549 cells, CD44 promotes migration, invasion, and apoptosis resistance, key hallmarks of lung adenocarcinoma progression. Disruption of CD44 in this polyclonal knockout impairs these phenotypes, facilitating dissection of its contributions to motility, matrix invasion, and EMT. The model also enables study of compensatory adhesion pathways and screening of CD44-targeted therapies.
This polyclonal knockout is suitable for hyaluronan binding assays, Transwell migration/invasion studies, wound healing, and phospho-signaling analysis via Western blot or flow cytometry. Researchers can examine CD44-dependent gene networks using RT-qPCR and co-immunoprecipitation, or explore tumor?Cstroma interactions in co-culture systems. It serves as an isogenic control for drug resistance screens and EMT research. For further details, contact Ascent Research.
