The DMD Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human ovarian carcinoma epithelial cell line A2780, targeting the DMD gene encoding dystrophin. This polyclonal pool contains diverse gene disruptions, providing a versatile loss-of-function model for studying dystrophin deficiency in epithelial contexts without clonal selection artifacts.
The A2780 cell line originates from an untreated ovarian endometrioid adenocarcinoma and is a standard model for epithelial ovarian cancer, employed in investigations of tumorigenesis, metastasis, and therapeutic resistance. Its well-defined epithelial phenotype and signaling networks make it an optimal host for examining dystrophin’s non-muscle roles.
DMD encodes dystrophin, a cytoskeletal protein that links actin filaments to the extracellular matrix via the dystrophin-glycoprotein complex (DGC), providing membrane stability and a signaling scaffold. Dystrophin interacts with dystroglycan, sarcoglycans, syntrophins, dystrobrevin, and nNOS. Expression is regulated by transcription factors such as MyoD, MEF2, and SRF, while downstream effects include nNOS localization, calcium homeostasis, MAPK signaling, NF-??B activation, and oxidative stress responses. The DGC thus integrates mechanotransduction, cell-matrix adhesion, and survival pathways.
In A2780 cells, dystrophin knockout disrupts DGC assembly, impairing membrane integrity and altering mechanosensitive signaling. This model enables dissection of dystrophin’s impact on epithelial adhesion, migration, and intracellular cascades, with potential relevance to cancer progression and metastasis. Loss of dystrophin may perturb nNOS-dependent signaling and calcium fluxes, affecting MAPK and NF-??B pathways.
This polyclonal knockout population is applicable in various advanced functional assays, including migration, invasion, and adhesion tests, to quantify cytoskeletal and adhesion changes. Molecular analyses such as western blotting, immunofluorescence, and co-immunoprecipitation can interrogate protein interactions, while phospho-signaling profiling and calcium imaging reveal altered signal transduction downstream of dystrophin loss. Transcriptomic studies via RNA-seq further characterize pathway alterations. The model supports drug screening for Duchenne muscular dystrophy therapies and mechanobiology research. For ordering or technical inquiries, contact Ascent Research.
