The ADAMTS14 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ADAMTS14 gene in the human esophageal squamous cell carcinoma cell line KYSE-150. This gene-edited product provides a loss-of-function model for studying ADAMTS14, a secreted procollagen N-proteinase critical for extracellular matrix (ECM) remodeling. The polyclonal format ensures a diverse knockout pool, enabling robust assessment of ADAMTS14-dependent phenotypes without clonal selection artifacts.
The KYSE-150 cell line, derived from a human esophageal squamous cell carcinoma, is a well-established model in cancer research. It retains characteristics of the original tumor, including aggressive growth behavior and invasion potential, making it suitable for investigating molecular mechanisms of esophageal cancer progression. KYSE-150 cells are frequently employed in studies of tumor biology, metastasis, and therapeutic resistance, providing a relevant context for examining the impact of ECM-related gene disruptions.
ADAMTS14 encodes a procollagen N-proteinase that specifically cleaves the amino-propeptides of procollagen I and II, a rate-limiting step in collagen fibril assembly. This processing is essential for mature collagen deposition and ECM organization. ADAMTS14 is transcriptionally regulated by TGF-beta signaling through the SMAD3/4 complex, and its activity directly contributes to TGF-beta activation by releasing the latent cytokine from ECM stores. Downstream, ADAMTS14-mediated collagen maturation modulates integrin signaling and ECM stiffness, influencing cell adhesion and migration. The enzyme interacts with its substrates procollagen I/II, fibronectin, and heparan sulfate proteoglycans, integrating mechanical cues with biochemical signaling. Representative pathway components include TGFBR, SMAD2/3, SMAD4, MMPs, and integrins, positioning ADAMTS14 at the intersection of collagen biosynthesis and TGF-beta bioavailability.
In KYSE-150 cells, ADAMTS14 knockout disrupts collagen processing and ECM remodeling, directly impacting the tumor microenvironment. Given the role of ADAMTS14 in activating TGF-beta, this knockout model enables dissection of TGF-beta-dependent and independent effects on esophageal carcinoma cell behavior. Loss of ADAMTS14 is anticipated to alter collagen fibril architecture, reduce integrin-mediated signaling, and impair invasive capacity. This model is particularly valuable for studying how ECM composition influences cancer metastasis and for validating ADAMTS14 as a potential therapeutic target in esophageal squamous cell carcinoma.
Researchers can utilize this polyclonal knockout population to investigate ADAMTS14 function in ECM regulation, collagen processing, and TGF-beta pathway modulation using assays such as Western blotting, RT-qPCR, immunofluorescence for collagen, and phospho-SMAD2 analysis. Functional studies may include Transwell migration/invasion assays, collagen gel contraction, and cell adhesion assays to evaluate metastatic potential. This product is also suitable for RNA-seq-based transcriptomic profiling to uncover downstream targets and for drug target validation screens. For customization or bulk orders, please contact Ascent Research.
