The ADAMTS14 Knockout AGS Polyclonal Cells are a heterogeneous population of AGS gastric adenocarcinoma cells subjected to CRISPR/Cas9-mediated disruption of the ADAMTS14 gene, creating a loss-of-function model for investigating extracellular matrix (ECM) remodeling and tumor progression. This polyclonal knockout cell pool retains genetic diversity, avoiding clonal artifacts and better reflecting the heterogeneous behavior of gastric tumors in experimental settings.
The AGS cell line, originally derived from a gastric adenocarcinoma of a 54-year-old female, is a well-established epithelial model in gastric cancer research. Its robust growth, defined signaling responses, and relevance to gastric carcinogenesis make it an ideal platform for gene perturbation studies, particularly those exploring tumor-microenvironment interactions and metastatic mechanisms.
ADAMTS14 encodes a secreted metalloproteinase that specifically cleaves the N-propeptides of procollagens I and III, an essential step for mature collagen fibril formation and ECM integrity. In this model, upstream regulators TGFB1 and IL1B modulate ADAMTS14 expression, while its proteolytic activity facilitates collagen binding to integrins such as ITGB1, triggering focal adhesion kinase (FAK) phosphorylation and subsequent activation of downstream effectors including SRC, ERK, and AKT. The knockout disrupts this cascade, attenuating collagen-integrin-FAK signaling. Interacting partners COL1A1, COL3A1, fibronectin (FN1), and the endogenous inhibitor TIMP3 further define the ADAMTS14-centered ECM regulatory network.
Within the gastric adenocarcinoma context, loss of ADAMTS14 compromises collagen processing, weakening the ECM scaffold that supports tumor cell adhesion, migration, and invasion. The resultant suppression of integrin/FAK signaling, along with altered TGF-beta and PI3K-Akt pathway activities, provides a controlled system to dissect how collagen remodeling contributes to tumor suppression and to evaluate the role of ECM dynamics in cancer progression.
Typical applications include wound healing and transwell invasion assays to assess metastatic potential, collagen gel contraction assays to quantify matrix remodeling, and phospho-FAK ELISA or western blotting to monitor signaling activity. These cells are also suited for screening anti-metastatic compounds and modeling the gastric tumor microenvironment. For further details, please contact Ascent Research.
