The ADAMTS14 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the ADAMTS14 gene in the SK-HEP-1 human liver adenocarcinoma cell line. This loss-of-function model is generated using CRISPR/Cas9-mediated gene editing to create a heterogeneous population of cells carrying targeted disruptions in ADAMTS14, enabling robust functional studies without clonal selection artifacts. The polyclonal format provides a representative pool of edited alleles, facilitating the investigation of gene function in a physiologically relevant context.
SK-HEP-1 is a widely utilized human hepatic adenocarcinoma cell line originally derived from the ascitic fluid of a patient with liver adenocarcinoma. These cells exhibit an adherent, epithelial-like morphology and possess both endothelial and mesenchymal characteristics, making them a versatile model for studying liver cancer biology, including tumor angiogenesis, epithelial-mesenchymal transition, and metastatic dissemination. The cell line??s dual endothelial and mesenchymal features render it particularly suitable for investigating extracellular matrix interactions and cell migration mechanisms.
ADAMTS14 encodes a secreted metalloproteinase that contains thrombospondin type-1 repeats and plays a critical role in extracellular matrix (ECM) remodeling by cleaving procollagens I, II, and III, as well as processing fibronectin and aggrecan. The protease is transcriptionally regulated by upstream factors such as TGF-beta, TNF-alpha, and IL-1 beta, and its activity is modulated by inhibitors like TIMP-3. Downstream, ADAMTS14-mediated proteolysis influences the pericellular ECM composition and stiffness, thereby impacting signaling cascades involving SMAD2, SMAD3, MAPK, NF-kappaB, and FAK. Knockout of ADAMTS14 abolishes this procollagen-processing function, leading to accumulation of unprocessed collagen fibrils, disrupted ECM organization, and altered cell adhesion and motility.
In SK-HEP-1 cells, ADAMTS14 knockout significantly compromises the cell line??s intrinsic mesenchymal characteristics, impairing its ability to remodel the ECM and migrate through collagen-rich matrices. This model is highly relevant for dissecting how tumor cells interact with the stromal microenvironment, particularly in the context of liver fibrosis and metastatic progression. The accumulation of uncleaved procollagen and changes in integrin-mediated adhesion pathways may suppress invasive behavior, making these cells a powerful tool for analyzing anti-invasive mechanisms and testing compounds that target ECM-driven tumor dissemination.
These polyclonal knockout cells are suited for a broad range of experimental applications, including Western blot analysis of ADAMTS14 expression, RT-qPCR quantification of procollagen and fibronectin genes, Transwell migration and invasion assays, gelatin zymography for matrix metalloproteinase activity, immunofluorescence imaging of ECM components, and cell adhesion studies. They facilitate drug screening efforts for anti-metastatic agents and enable detailed functional studies of ECM remodeling in liver cancer and fibrosis models. For further technical information and support, please contact Ascent Research.
