The DMD Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric epithelial cell line. This product features targeted disruption of the DMD gene, which encodes the large cytoskeletal scaffold protein dystrophin. The polyclonal knockout population provides a heterogeneous loss-of-function model for studying dystrophin-dependent processes in a gastric epithelial context. Unlike clonal isolates, polyclonal knockout cells preserve a broad distribution of genetic backgrounds, enabling robust assessment of gene function across a diverse cellular pool while minimizing clonal selection artifacts.
The AGS parental cell line originates from a human gastric adenocarcinoma and serves as a widely used model for gastric mucosal epithelial biology. These cells recapitulate key features of gastric epithelial cells, including secretion competence and barrier-forming potential, making them particularly relevant for investigations into gastric pathophysiology. The AGS line??s epithelial origin and transformed nature allow researchers to examine how dystrophin loss influences epithelial cell adhesion, migration, and tumor-associated behaviors within the gastrointestinal microenvironment.
Dystrophin, encoded by DMD, is a critical scaffold protein of the dystrophin-glycoprotein complex (DGC). It connects the actin cytoskeleton to the extracellular matrix via interactions with ??-dystroglycan, sarcoglycans, syntrophins, and ??-dystrobrevin, thereby stabilizing the plasma membrane. In muscle, this complex is essential for sarcolemma integrity; in epithelial cells, it influences cell adhesion and mechanosignaling. Dystrophin also tethers nNOS, modulating nitric oxide production. The DMD gene is regulated by transcription factors MEF2, SP1, and CREB, and its disruption compromises DGC assembly, impacting downstream pathways involving laminin-2 and integrin signaling.
In AGS gastric epithelial cells, DMD knockout is expected to disrupt cell-matrix adhesion and mechanosignaling, processes vital for epithelial homeostasis and tumor progression. Loss of dystrophin may weaken cell-extracellular matrix connections, potentially altering migration, invasion, and responses to mechanical cues. This model thus provides a tool to investigate dystrophin’s roles in epithelial tumor biology beyond its classical muscle functions, particularly in gastric cancer.
This polyclonal knockout pool supports diverse applications, including muscular dystrophy studies in non-muscle lineages, gene therapy testing, and cancer cell adhesion and migration research. Typical assays include western blotting and immunofluorescence for dystrophin loss, migration and invasion assays, and RT-qPCR or RNA-seq for downstream pathway analysis. By using AGS cells, researchers can study dystrophin deficiency in gastric epithelial malignancy and identify therapeutic targets. For further details, please contact Ascent Research.
