The DSG2 Knockout A2780 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal population in which the DSG2 gene has been disrupted in the A2780 ovarian carcinoma line. This loss-of-function model enables investigation of desmoglein-2 in cell adhesion and signaling, and the heterogeneous polyclonal format avoids clonal bias, making it well-suited for population-based assays.
The A2780 host cell line is a human ovarian epithelial carcinoma line with adherent morphology, widely used to study ovarian tumorigenesis and chemoresistance. It retains key oncogenic features, providing a relevant background for functional analysis of adhesion molecules and pathways driving metastasis and drug sensitivity.
DSG2 encodes a calcium-dependent cadherin that forms desmosomal junctions through homophilic and heterophilic interactions. Its direct binding partners include plakoglobin (JUP), plakophilin-2 (PKP2), desmoplakin (DSP), and desmocollin-2 (DSC2). Upstream, it is regulated by p63, Snail, Slug, EGFR, and ADAM10/ADAM17-mediated ectodomain shedding. DSG2 disruption impairs desmosome integrity, redistributes plakoglobin and beta-catenin, and modulates Wnt target genes such as MYC and CCND1, thereby linking cell adhesion to growth control.
In the A2780 ovarian cancer context, DSG2 knockout is expected to weaken intercellular adhesion, disrupt desmosome assembly, and potentially promote an epithelial-mesenchymal transition (EMT)-like state, enhancing migratory and invasive capacity. These changes may also alter cellular responses to chemotherapeutics, informing studies on drug resistance. Additionally, this model can provide mechanistic insights into desmosome-related diseases such as arrhythmogenic right ventricular cardiomyopathy and pemphigus.
Typical applications include immunofluorescence localization of desmosomal components, cell aggregation and dissociation assays to quantify adhesion strength, and barrier integrity measurements using transepithelial electrical resistance (TEER). Migration and invasion assays, co-immunoprecipitation of protein complexes, and expression analysis by RT-qPCR and Western blotting enable dissection of EMT and Wnt signaling. Apoptosis assays can assess drug sensitivity changes. For further information, contact Ascent Research.
