The DSG2 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of HeLa cells with targeted disruption of the DSG2 gene, generating a loss-of-function model. Supplied as a heterogeneous pool without clonal isolation, this population maintains the parental HeLa genetic background while eliminating desmoglein-2 expression. The polyclonal format preserves natural variability, reducing selection pressure and enabling pooled knockout phenotype studies. By avoiding single-cell cloning, it reduces the risk of clonal artifacts and enables robust, reproducible experiments.
HeLa cells are an immortalized human cervical epithelial line derived from a cervical adenocarcinoma and positive for HPV18. Widely used in biomedical research, they offer robust growth and extensive molecular characterization. Their cancer origin causes altered adhesion and signaling, making them a relevant model for oncology. They retain key junctional proteins like desmogleins and desmocollins, providing a suitable context for desmosome studies.
DSG2 encodes desmoglein-2, a calcium-dependent desmosomal cadherin that mediates cell?Ccell adhesion and links to intermediate filaments via plakoglobin (JUP), plakophilin-2 (PKP2), and desmoplakin (DSP). Upstream regulators include p53, ??-catenin/TCF, EGF receptor, and cytokines TNF-?? and IL-1??; downstream, DSG2 affects localization of JUP, DSP, PKP2, and actin reorganization. Its disruption impairs desmosome assembly, weakens adhesion, and dysregulates Wnt/??-catenin signaling, promoting barrier dysfunction and invasiveness.
In HeLa cells, DSG2 knockout amplifies adhesion defects due to their transformed nature, making it a potent model for studying desmosome-dependent processes. It enables investigation of collective migration, invasion, and mechanics, while probing cancer-relevant pathways like Wnt/??-catenin. The polyclonal population is suited for assays such as TEER and 3D invasion where pooled phenotypes reveal dominant effects. This approach avoids clonal bias and better represents the heterogeneous response of a cancer cell population.
This knockout model is ideal for epithelial barrier studies (TEER), desmosome assembly (immunofluorescence), adhesion assays (hanging drop), and migration/wound healing. Protein interactions can be validated by western blotting and co-immunoprecipitation; flow cytometry assesses surface DSG2 loss; RNA-seq profiles transcriptomes. It also serves drug screening for adhesive disorders and metastasis. Additionally, co-culture with other cell types can be employed to study heterotypic adhesion. For further details or custom solutions, please contact Ascent Research.
