The ADAMTS14 Knockout HGC-27 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal cell population generated from the HGC-27 human gastric adenocarcinoma epithelial cell line. This heterogeneous pool carries targeted disruptions of the ADAMTS14 gene, resulting in a permanent loss-of-function model. The polyclonal format preserves the natural diversity of knockout events, enabling robust analysis of ADAMTS14-dependent phenotypes without clonal selection, ideal for investigating its roles in extracellular matrix regulation and gastric cancer biology.
The parental HGC-27 cell line is derived from a lymph node metastasis of a human gastric adenocarcinoma and exhibits poor differentiation and aggressive tumorigenic properties. It is a widely used model for gastric cancer progression and metastasis, maintaining key features of tumor?Cstromal interactions and invasive behavior. HGC-27 cells are adherent and epithelial, with demonstrated metastatic potential in vitro and in vivo, making them ideal for studying gastric cancer cell dissemination.
ADAMTS14 encodes a secreted metalloprotease that functions as a procollagen N-proteinase, cleaving the N-propeptides of type I and II procollagens to facilitate collagen fibril assembly and extracellular matrix (ECM) organization. Its activity is regulated upstream by TGFB1, mechanical stress, and hypoxia, and it acts within a pathway involving COL1A1, COL2A2, TGFB1, and SMAD2/3. Downstream, ADAMTS14-mediated collagen maturation influences integrin signaling and ECM remodeling, processes critical for tumor microenvironment stiffness, cell adhesion, and metastatic progression in gastric cancer.
Ablating ADAMTS14 in HGC-27 cells creates a model to dissect the connection between collagen processing and gastric cancer invasion. Loss of ADAMTS14 function impairs procollagen cleavage, causing defective collagen fibrillogenesis and altered ECM architecture, which can disrupt cell adhesion and mechanotransduction. This polyclonal knockout population is valuable for examining how ECM remodeling defects influence the metastatic phenotype of gastric adenocarcinoma cells and for testing whether collagen maturation status modulates signaling pathways that drive tumor progression, leveraging heterogeneous responses for robust phenotype identification.
This knockout product supports diverse applications, including analysis of collagen maturation in cancer stroma, functional studies of ECM remodeling in gastric cancer metastasis, and investigation of ADAMTS14-dependent tumor microenvironment interactions. Recommended assays encompass western blotting for ADAMTS14 and collagen intermediates, RT-qPCR for collagen genes, immunofluorescence for collagen deposition, migration/invasion assays, collagen gel contraction, and RNA-seq profiling. These approaches enable comprehensive interrogation of ADAMTS14-mediated pathways. For inquiries or pricing, contact Ascent Research.
