The DTNA Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population derived from the A2780 human ovarian adenocarcinoma cell line. This product introduces a genetic disruption of the DTNA gene, encoding dystrobrevin-alpha, a scaffolding protein integral to cytoskeletal anchoring and signal transduction. The polyclonal format provides a heterogeneous, loss-of-function model that retains the genetic diversity of the edited pool, suitable for probing the functional consequences of DTNA ablation in ovarian cancer biology.
The A2780 cell line was originally established from an untreated patient with ovarian endometrioid adenocarcinoma and has become a cornerstone model for studying ovarian cancer progression, drug resistance, and metastasis. As an epithelial ovarian cancer line, A2780 cells exhibit robust cell?Ccell and cell?Cextracellular matrix (ECM) interactions, making them particularly suited for investigating adhesion and migration mechanisms. The intact dystrophin-glycoprotein complex in wild-type A2780 cells maintains membrane integrity and facilitates signaling events downstream of integrin activation. Disruption of DTNA in this context allows researchers to dissect the contribution of dystrobrevin-alpha to ovarian tumor cell behavior.
DTNA-encoded dystrobrevin-alpha functions as a key scaffold within the dystrophin-glycoprotein complex (DGC), directly interacting with dystrophin, utrophin, syntrophins, dysbindin, and sarcoglycans. This complex connects the intracellular actin cytoskeleton to the ECM via laminin-??2 (LAMA2) and ??-dystroglycan (DAG1). Dystrobrevin-alpha is activated by integrin-mediated extracellular matrix signals and transmits mechanical cues downstream to regulate actin filament organization, syntrophin recruitment, and nNOS signaling. In epithelial cells like A2780, DTNA governs cell adhesion and cytoskeletal dynamics; its knockout disrupts these interactions, altering focal adhesion turnover and actin remodeling.
In the A2780 ovarian cancer model, loss of dystrobrevin-alpha disrupts cell?CECM adhesion and weakens the linkage between the actin cytoskeleton and dystroglycan complexes, impairing responses to matrix stiffness. This destabilization alters focal adhesion kinase and integrin signaling, reducing migration and invasion capacity. Consequently, the DTNA knockout polyclonal population provides a system to study DGC-associated scaffolding in ovarian carcinoma dissemination and mechanotransduction, helping to elucidate how cytoskeletal anchoring proteins influence peritoneal metastasis.
Researchers can employ the DTNA Knockout A2780 Polyclonal Cells in a variety of functional experiments, including quantitative cell adhesion assays on ECM substrates (e.g., laminin, fibronectin) to assess integrin-mediated attachment, wound healing migration assays to measure collective cell motility, and immunofluorescence staining of actin filaments and focal adhesion markers (e.g., vinculin, paxillin) for high-resolution cytoskeletal analysis. Flow cytometry or Western blotting confirms efficient disruption of dystrobrevin-alpha expression. These polyclonal knockout cells are also amenable to co-culture and drug response studies where DGC integrity may influence chemosensitivity. For further technical details, please contact Ascent Research.
