The DLG1 Knockout AGS Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal knockout population of AGS human gastric adenocarcinoma cells. This heterogeneous pool contains diverse genetic disruptions at the DLG1 locus, generated without clonal selection, thereby preserving population-level variability that mirrors the cellular heterogeneity observed in tumor tissues. It serves as a robust loss-of-function model for investigating ensemble cellular behaviors upon DLG1 ablation.
The parental AGS cell line is an adherent, epithelial-like line derived from a gastric adenocarcinoma of a 54-year-old female. Widely employed as a model for gastric cancer, intestinal metaplasia, and Helicobacter pylori infection, AGS cells retain key signaling and adhesion properties of gastric epithelium. Their established use in drug response studies and host?Cpathogen research makes them a relevant platform for examining tumor-suppressive mechanisms.
DLG1 encodes a membrane-associated guanylate kinase scaffold that organizes adherens and tight junction complexes, linking E-cadherin and cortical actin. It directly interacts with APC, PTEN, and ??-catenin, thus restricting Wnt/??-catenin and Hippo/YAP signaling at the membrane. Through PDZ domains, DLG1 assemblies include DLGAPs, CASK, LIN7, and MPP proteins. Its localization is modulated by upstream cues such as Wnt ligands, calcium influx, and SRC kinases, while downstream it regulates RhoA via LARG and p38 MAPK, ultimately controlling YAP/TAZ and TCF/LEF transcriptional outputs.
In gastric cancer, DLG1 acts as a tumor suppressor; its loss disrupts junctional integrity, permitting ??-catenin nuclear translocation and YAP/TAZ activation, which fuel proliferation, migration, and epithelial-to-mesenchymal transition. The AGS background, with its intrinsic pathway activation, recapitulates these events, enabling dissection of how DLG1 deficiency drives gastric adenocarcinoma progression and influences responsiveness to therapeutic agents.
This polyclonal knockout model is suited for elucidating DLG1??s tumor-suppressive functions in gastric cancer, exploring epithelial polarity and junctional signaling, and screening inhibitors of Wnt/Hippo pathways. Experimental approaches include Western blotting for DLG1, ??-catenin, and YAP; immunofluorescence for tight junction markers; TCF/LEF luciferase assays; transwell migration/invasion tests; co-immunoprecipitation with APC and PTEN; and RNA-seq transcriptome analyses. It also facilitates investigation of H. pylori-induced junctional remodeling. For additional information or custom solutions, contact Ascent Research.
