This product is a CRISPR/Cas9-edited polyclonal knockout cell population in which the DSC2 gene has been disrupted via CRISPR/Cas9-mediated genome editing. The polyclonal format represents a heterogeneous pool of AGS cells, each carrying distinct editing events, providing a biologically relevant loss-of-function model without assuming clonal uniformity.
The parental AGS cell line is a well-characterized epithelial model derived from the gastric adenocarcinoma of a 54-year-old female. AGS cells retain key features of gastric epithelial cancer, including adherent growth and responsiveness to oncogenic stimuli, making them a widely used system for studying signaling pathways and metastatic mechanisms in gastric cancer. The cell line is also responsive to stimuli such as EGF and TGF-??1, which are relevant to EMT induction.
DSC2 encodes desmocollin 2, a calcium-dependent cadherin that is an essential component of desmosomal junctions, mediating strong cell-cell adhesion in epithelial tissues. Within desmosomes, DSC2 interacts with desmoglein 2, plakoglobin (JUP), plakophilin 2 (PKP2), and desmoplakin (DSP) to form adhesive complexes. DSC2 is transcriptionally regulated by Wnt ligands such as Wnt3a, EGF, and TGF-??1 through ??-catenin/TCF complexes. Loss of DSC2 can liberate ??-catenin (CTNNB1) from junctional pools, promoting its nuclear translocation and activation of TCF/LEF target genes including c-MYC and CCND1. Furthermore, DSC2 knockout upregulates matrix metalloproteinases MMP2 and MMP9 and EMT transcription factors SNAI1 and ZEB1, which collectively drive invasive behavior.
In AGS gastric cancer cells, DSC2 disruption profoundly impacts desmosome assembly and epithelial integrity. The loss of desmocollin 2 weakens intercellular adhesion, facilitating a more migratory and invasive phenotype. By perturbing the balance of ??-catenin trafficking, this knockout model enhances Wnt/??-catenin-dependent transcriptional programs that promote epithelial-mesenchymal transition and confer increased metastatic potential, making it a valuable system for dissecting the molecular links between desmosomal dysfunction and gastric cancer progression.
Typical research applications include investigation of desmosome-mediated adhesion in gastric cancer, elucidation of Wnt/??-catenin signaling regulation, drug target validation for anti-metastatic therapies, and modeling aspects of arrhythmogenic right ventricular cardiomyopathy within an epithelial framework. Compatible assays encompass western blotting for DSC2, ??-catenin, and EMT markers; RT-qPCR for DSC2 and Wnt target genes; immunofluorescence to assess desmosome integrity; cell migration and invasion assays; co-immunoprecipitation of desmosomal complexes; phospho-signaling analysis; and transcriptomic profiling via RNA-seq. For additional information or to discuss custom cell engineering services, please contact Ascent Research.
