The DMD Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the HGC-27 human gastric carcinoma cell line, featuring targeted disruption of the DMD gene. This loss-of-function model abolishes dystrophin expression in a heterogeneous knockout pool, enabling robust population-level analyses without clonal selection biases.
HGC-27 is an adherent epithelial cell line originated from a lymph node metastasis of a gastric carcinoma. Its aggressive metastatic background makes it a relevant model for studying gastric cancer progression and dissemination. The cells retain key oncogenic features and are widely employed to investigate mechanisms of invasion, migration, and response to therapeutics in advanced gastric adenocarcinoma.
DMD encodes dystrophin, a large subsarcolemmal protein that forms the core of the dystrophin-glycoprotein complex (DGC), linking intracellular actin filaments to the extracellular matrix via laminin?211. Dystrophin directly binds actin and ???dystroglycan, and scaffolds syntrophins, ???dystrobrevin, and sarcoglycans to stabilize the membrane and organize signaling molecules such as nNOS. In gastric cancer, DMD expression is frequently suppressed by methylation silencing and is modulated by Hippo pathway effectors YAP/TAZ. Loss of dystrophin disrupts DGC integrity, leading to altered focal adhesion dynamics and altered PI3K?Akt and Hippo signaling. This molecular network positions dystrophin as a potential tumor suppressor whose inactivation promotes actin cytoskeleton reorganization, reduced cell?matrix adhesion, and enhanced invasive behavior.
In the HGC-27 metastatic background, DMD knockout models the consequences of dystrophin loss in gastric carcinoma, where it has been associated with poor prognosis and increased metastatic potential. The model is particularly suited for dissecting how DGC dysfunction cooperates with oncogenic pathways to drive epithelial?mesenchymal transition, collective migration, and distant colonization. It also enables exploration of synthetic lethalities and epigenetic reactivation strategies within a clinically relevant late?stage cancer context.
Key applications include western blot and RT?qPCR for confirming dystrophin ablation, immunofluorescence evaluation of DGC component localization, transwell migration/invasion assays, apoptosis quantification, and phospho?profiling to map pathway alterations. Co?immunoprecipitation experiments can assess residual complex formation, while synthetic lethal screens or drug testing may identify novel targets. This product is also suitable for evaluating demethylating agents or YAP/TAZ inhibitors. For additional details, please contact Ascent Research.
