The DSG2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to eliminate functional expression of the DSG2 gene in the AGS human gastric adenocarcinoma epithelial background. This cell pool, generated via CRISPR/Cas9-mediated gene disruption, comprises a heterogeneous mix of DSG2-null and edited genotypes, bypassing clonal selection artifacts and preserving polyclonal complexity for population-level studies. The product provides researchers with a robust loss-of-function model to interrogate desmoglein 2 biology without the constraints of single-cell clonal variation, and is supplied as a ready-to-use cryopreserved stock suitable for direct experimental applications in cancer signaling, adhesion biology, and drug discovery.
The host AGS cell line is a widely utilized model of human gastric adenocarcinoma, derived from a metastatic tumor and characterized by adherent epithelial morphology. AGS cells retain several features of gastric epithelium and are extensively employed to dissect mechanisms underlying gastric cancer progression, including tumor cell invasion, metastasis, and drug resistance. Their tractable in vitro culture and well-characterized signaling networks make them an ideal system for investigating the functional consequences of DSG2 ablation in the context of gastric malignancies, where desmoglein 2 dysregulation is increasingly linked to aggressive disease.
DSG2 encodes desmoglein 2, a calcium-dependent cadherin family member essential for desmosome-mediated intercellular adhesion. It functions as a transmembrane glycoprotein that connects neighboring epithelial cells by partnering with desmosomal plaque proteins such as plakoglobin, desmoplakin, and plakophilin-2. Beyond structural adhesion, DSG2 participates in signal transduction, particularly in modulating the Wnt/??-catenin pathway. Its knockout disrupts desmosome integrity, liberating ??-catenin from junctional complexes and promoting its nuclear translocation. DSG2 is transcriptionally repressed by epithelial-mesenchymal transition (EMT)-inducing factors TGF-??, Snail, Slug, and p63, and its loss can phenocopy EMT by upregulating mesenchymal markers (Vimentin) and downregulating epithelial markers (E-cadherin). Downstream, increased ??-catenin signaling activates target genes such as MYC and CCND1, while the destruction complex component GSK3?? and TCF/LEF transcription factors further propagate oncogenic transcriptional programs.
In the AGS gastric cancer context, DSG2 knockout generates a disease-relevant platform to study the loss of cell-cell adhesion and its contribution to malignant phenotypes. Since AGS cells originally express DSG2, its deletion recreates a scenario observed in certain gastric carcinomas where desmoglein 2 downregulation correlates with invasiveness. The resulting model allows dissection of how adhesion defects trigger EMT-like transitions, enhance migratory and invasive capacity, and potentially alter sensitivity to chemotherapeutic agents. This system is thus invaluable for exploring the molecular underpinnings of gastric cancer metastasis and for identifying therapeutic vulnerabilities associated with desmosomal dysfunction.
This polyclonal knockout pool is suited for a broad panel of analytical techniques including Western blotting, immunofluorescence, transwell migration and invasion assays, RT-qPCR, Wnt/??-catenin luciferase reporter assays, co-immunoprecipitation, phospho-signaling pathway arrays, and drug sensitivity profiling. Key research applications encompass gastric cancer metastasis studies, EMT pathway analysis, investigation of drug resistance mechanisms, and characterization of cell adhesion defects in cancer. For further technical details or to discuss custom screening strategies, please contact Ascent Research.
