The ADAMTS14 Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the TE1 human esophageal squamous cell carcinoma epithelial cell line, in which the ADAMTS14 gene is disrupted to ablate procollagen N-proteinase activity. The polyclonal nature ensures a diverse spectrum of gene disruptions, providing a robust tool for functional genomics and loss-of-function investigations in a cancer-relevant context.
The TE1 host cell line is a well-differentiated human esophageal squamous cell carcinoma epithelial model extensively used in cancer biology and extracellular matrix research. These adherent cells retain key malignant characteristics, including deregulated proliferation and migratory capacity, making them ideal for studying invasion and metastasis mechanisms and the role of ECM-modifying enzymes in tumor progression.
ADAMTS14 encodes a procollagen N-proteinase that cleaves amino-propeptides of procollagen types I, II, and III, enabling maturation of collagen monomers and fibril formation. Its activity is regulated by TGF-??, inflammatory cytokines, and mechanical stress. The enzyme directly interacts with procollagens and fibronectin, and its action generates mature collagen fibrils that engage integrin receptors, triggering downstream signaling. Loss of ADAMTS14 disrupts collagen fibrillogenesis, leading to aberrant ECM architecture and altered cell-matrix communication.
In the TE1 background, ADAMTS14 knockout impairs conversion of procollagen to collagen, compromising ECM integrity and affecting cell adhesion, migration, and invasion??processes central to esophageal carcinoma progression. This model enables dissection of ADAMTS14??s contribution to integrin-mediated signaling and tumor cell behavior within a physiologically relevant epithelial cancer system. It also permits interrogation of how mechanical cues and cytokine signaling intersect with ADAMTS14 function to modulate the tumor microenvironment.
This product supports diverse applications, including ECM remodeling studies, cancer invasion modeling, collagen maturation analysis, and drug screening for connective tissue disorders. Representative assays include Western blotting, collagen maturation assays, migration/invasion assays, immunofluorescence for ECM components, RNA-seq, and co-immunoprecipitation. For further technical details or to discuss experimental design, please contact Ascent Research.
