DTNB Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the DTNB gene has been disrupted via CRISPR/Cas9-mediated genome editing. This human ovarian carcinoma A2780 cell-based model provides a powerful tool for studying the loss of function of beta-dystrobrevin, the scaffold protein encoded by DTNB. The polyclonal nature of the knockout pool ensures representation of diverse editing events, facilitating robust analysis of gene disruption phenotypes without clonal bias.
The A2780 cell line is a human ovarian carcinoma epithelial line derived from an untreated patient and is well characterized for its cisplatin sensitivity. It is extensively employed as a model system for ovarian tumor biology, drug resistance mechanisms, and metastatic progression. Its epithelial origin and intact adhesive properties make it particularly suitable for investigating cell?Cmatrix interactions and signaling pathways relevant to ovarian cancer.
DTNB encodes beta-dystrobrevin, a core component of the dystrophin glycoprotein complex (DGC) that functions as a structural and signaling scaffold. It connects the actin cytoskeleton to the extracellular matrix via dystrophin/utrophin and sarcoglycans, while also recruiting signaling proteins including nNOS and GRB2. Upstream, integrin-mediated adhesion and mechanical tension regulate DGC integrity. Downstream, DTNB knockout perturbs nNOS localization and GRB2-mediated MAPK signaling, ultimately affecting actin remodeling. Additional interacting partners like syntrophin and dystrobrevin-binding protein 1 further integrate mechanical and biochemical cues.
In the context of ovarian carcinoma, cell?Cmatrix adhesion is critical for invasion and metastasis. The A2780 cell line, when depleted of DTNB, offers a physiologically relevant platform to dissect how loss of dystrobrevin-mediated scaffolding impairs adhesion, migration, and survival signaling. Since the DGC contributes to membrane stability and downstream effector recruitment, its disruption may sensitize tumor cells to chemotherapeutic agents such as cisplatin, providing insights into drug resistance mechanisms and potential therapeutic vulnerabilities in cancers associated with aberrant dystrophin complex function.
This polyclonal knockout pool is ideally suited for applications including cell adhesion assays, transwell migration and invasion assays, and phospho-signaling pathway analysis (e.g., monitoring GRB2?CMAPK axis activation) to elucidate beta-dystrobrevin??s role in ovarian cancer progression. It can also be used in cisplatin sensitivity profiling and high-throughput screening for compounds targeting dystrophin complex-related pathways. Standard validation assays such as western blotting and immunofluorescence confirm knockout efficacy. For additional information or to discuss custom cell engineering projects, please contact Ascent Research.
