The ADAMTS14 Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal cell population in which the ADAMTS14 gene has been disrupted, generating a loss-of-function model in a human ovarian cancer background. This polyclonal pool, rather than a clonally derived line, provides a heterogeneous knockout cell population suitable for studying ADAMTS14-dependent processes without the biases of single-cell selection. The product is intended for researchers investigating the roles of ADAMTS14 in extracellular matrix (ECM) remodeling, cell migration, and tumor-stroma interactions.
The parental A2780 cell line is a well-characterized human ovarian endometrioid carcinoma model derived from an untreated patient. These epithelial cells are cisplatin-sensitive and widely employed to study ovarian cancer biology, including tumor progression, metastasis, and drug response. Their robust growth and defined signaling properties make them a reliable platform for gene perturbation studies, especially in the context of ECM-related oncogenic mechanisms.
ADAMTS14 encodes a secreted metalloprotease that specifically cleaves the N-propeptides of procollagen types I and III, a critical step in collagen fibrillogenesis and ECM assembly. Its expression is transcriptionally regulated by upstream factors such as TGFB1, IL1B, and HIF1A. Downstream, mature collagen type I and type III engage integrin receptors, notably integrin ??2??1, leading to activation of FAK and Src signaling cascades. ADAMTS14 also interacts with TIMP-3, which modulates its activity, and its function is embedded within a broader network involving TGFB1?CSMAD2/3, procollagen I processing, collagen crosslinking by LOX enzymes, and RhoA-mediated cytoskeletal reorganization.
In the A2780 context, ADAMTS14 knockout impairs procollagen processing, leading to disrupted extracellular matrix assembly and attenuated integrin-mediated signaling. According to the mechanistic model, this deficiency reduces cell migration and invasion potential while altering tumor microenvironment interactions, potentially impacting ovarian cancer metastasis and cisplatin sensitivity. The loss of ADAMTS14 may shift the balance of ECM turnover, lowering the availability of mature collagen fibers that support invasive protrusions and adhesion-dependent survival signals.
This polyclonal knockout cell population is suited for a broad range of experimental applications, including tumor microenvironment research, metastasis and invasion assays using Boyden chambers, cell adhesion studies, immunofluorescence analysis of collagen deposition, proliferation assays, and cisplatin sensitivity testing. Comparative transcriptomic profiling by RNA-seq can further elucidate the global impact of ADAMTS14 loss. These cells thus provide a powerful tool for dissecting ADAMTS14-dependent pathways in ovarian cancer pathophysiology and for identifying novel therapeutic targets. For detailed product information and technical support, please contact Ascent Research.
