The ADAMTS14 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma epithelial cell line. This product features CRISPR/Cas9-mediated disruption of the ADAMTS14 gene, generating a heterogeneous population of cells with loss-of-function of the target gene. The polyclonal format maintains the inherent genetic diversity of the parental line, offering a robust and physiologically relevant model for investigating ADAMTS14-dependent processes.
The host A-549 cell line was originally isolated from a 58-year-old male patient with lung adenocarcinoma and exhibits characteristics of type II pneumocytes. As a widely used epithelial model, A-549 cells recapitulate key features of the alveolar epithelium and are responsive to TGF-?? stimulation, actively producing collagen and other extracellular matrix components. This background makes them particularly well-suited for studying genes involved in extracellular matrix remodeling within the context of lung cancer biology.
ADAMTS14 encodes a secreted metalloprotease that specifically cleaves the N-propeptides of procollagens I and III, a rate-limiting step in collagen fibrillogenesis. Its expression is stimulated by TGF-??1, IL-1??, and mechanical stress through the TGF-?? receptor?CSMAD2/3 signaling axis, and its activation requires proteolytic processing by furin. Downstream, mature collagen I and III assemble into fibrils that modulate extracellular matrix stiffness and cell adhesion molecules, with fibronectin and heparin serving as key interactors that further regulate matrix organization. Thus, ADAMTS14 integrates upstream signals to control collagen assembly and tissue mechanical properties.
Disrupting ADAMTS14 in the A-549 background allows detailed dissection of how defective procollagen processing affects lung adenocarcinoma progression. Given that A-549 cells contribute to desmoplastic reactions and TGF-??-driven epithelial?Cmesenchymal transition programs, this knockout model reveals the functional consequences of impaired collagen maturation on tumor cell migration, invasion, and matrix stiffening. The polyclonal nature reflects the heterogeneity observed in patient tumors, enhancing translational relevance for studies of tumor microenvironment dynamics.
This polyclonal knockout is suitable for a broad range of functional assays, including procollagen cleavage analysis, collagen gel contraction, transwell migration and invasion assays, and immunofluorescence staining of extracellular matrix proteins. It enables researchers to explore ADAMTS14-dependent mechanisms in tumor invasion, metastasis, and fibrosis modeling, as well as to screen ECM-targeted therapeutics in a population-based context. For additional details or technical inquiries, please contact Ascent Research.
