The DSG2 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the human gastric cancer cell line HGC-27 with targeted disruption of the DSG2 gene. This polyclonal pool introduces loss-of-function mutations via CRISPR/Cas9, providing a physiologically relevant model to study desmosomal cadherin function without clonal artifacts. The heterogeneous knockout population captures diverse genetic alterations, mimicking tumor heterogeneity and minimizing clonal biases inherent in single-cell clones.
HGC-27 is a poorly differentiated gastric adenocarcinoma cell line derived from a lymph node metastasis, widely used to model metastatic gastric cancer. These cells exhibit enhanced migratory and invasive behavior, deregulated proliferation, and aberrant signaling, reflecting advanced disease. The metastatic origin makes HGC-27 particularly suitable for investigating molecular mechanisms of tumor dissemination and therapeutic resistance.
Desmoglein-2, encoded by DSG2, is a calcium-dependent cadherin that assembles into desmosomes together with desmocollin-2 (DSC2), plakoglobin (JUP), plakophilin-2 (PKP2), and desmoplakin (DSP) to maintain epithelial integrity. Its expression is controlled by upstream regulators including TP63, ??-catenin (CTNNB1), and TGF-??, and it interacts functionally with EGFR signaling. DSG2 knockout disrupts desmosomal adhesion, liberating plakoglobin to modulate Wnt/??-catenin transcriptional activity and activating Rho GTPase-mediated cytoskeletal rearrangements. This loss of adhesion primes cells for enhanced motility and epithelial-mesenchymal transition (EMT), a key step in metastasis.
In HGC-27 cells, DSG2 ablation synergizes with the inherently aggressive background to exaggerate phenotypes such as reduced cell-cell adhesion, increased migration, invasion, and altered drug sensitivity. The model provides a powerful tool to dissect the role of desmosomal dysfunction in gastric cancer progression and to explore therapeutic strategies targeting adhesion-related pathways. Crosstalk between DSG2 loss, EGFR activation, and ??-catenin signaling offers insights into mechanisms driving EMT and drug resistance.
This polyclonal knockout cell pool is validated for use in Western blotting, RT-qPCR, immunofluorescence, and functional assays including adhesion, Transwell migration/invasion, wound healing, co-immunoprecipitation, and drug sensitivity testing. Researchers investigating desmosome biology, gastric cancer metastasis, or EMT can employ this model to delineate how loss of desmoglein-2 impacts malignant behavior. For further information, please contact Ascent Research.
