The DSC2 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HGC-27 human gastric adenocarcinoma epithelial cells engineered to disrupt the DSC2 gene, which encodes the desmosomal cadherin desmocollin-2. This loss-of-function model is designed for advanced investigation of cell-cell adhesion, desmosome architecture, and the contribution of desmosomal components to signaling networks that drive tumor progression and metastasis. By generating a heterogeneous knockout cell pool, this product enables robust functional studies without relying on a single clonal isolate, thereby reflecting the genetic variability inherent in cancer cell populations.
The HGC-27 parental cell line was originally established from a lymph node metastasis of a human gastric adenocarcinoma, providing a highly relevant in vitro system that recapitulates invasive and metastatic phenotypes. These epithelial cells are widely used to explore molecular mechanisms of gastric cancer dissemination, including enhanced migratory capacity, extracellular matrix degradation, and colonization at secondary sites. Their metastatic origin makes them especially suited for loss-of-function studies targeting adhesion molecules that normally constrain tumor cell spread.
Desmocollin-2 is a critical component of desmosomes, mediating calcium-dependent homophilic and heterophilic interactions with desmoglein-2 to maintain strong intercellular cohesion. Intracellularly, it associates with plakoglobin, plakophilin-2, and desmoplakin, which link the adhesive complex to keratin intermediate filaments. DSC2 transcription is regulated by p63 and AP-1 transcription factors, and its expression responds to Wnt/??-catenin signaling and EGF stimulation. Disruption of DSC2 can destabilize desmosomal junctions, liberate plakoglobin to modulate ??-catenin transcriptional activity, and potentially shift the balance toward a more motile and invasive phenotype through crosstalk with Wnt/??-catenin target genes.
In the context of HGC-27 cells, ablation of DSC2 provides a pathologically relevant model to examine how loss of desmosomal adhesion contributes to gastric adenocarcinoma aggressiveness. Because these cells inherently possess invasive traits, eliminating a key adhesion receptor allows researchers to dissect the interplay between mechanical junction integrity and prometastatic signaling pathways. The model can also be used to evaluate drug sensitivities that depend on cell-cell contact status, as well as to screen for compounds that selectively target tumor cells with compromised desmosomal function.
Researchers can utilize these polyclonal knockout cells in a range of downstream assays, including Western blotting and RT-qPCR to verify gene disruption, immunofluorescence to assess desmosome organization, and cell aggregation or migration/invasion assays to quantify functional changes. Wnt/??-catenin reporter assays enable direct measurement of pathway activation, while co-culture or three-dimensional invasion models extend the relevance to complex tumor microenvironments. For additional technical specifications or ordering information, please contact Ascent Research.
