The DTNA Knockout MES-OV Polyclonal Cells product consists of a polyclonal population of MES-OV cells that have undergone CRISPR/Cas9-mediated disruption of the DTNA gene, generating a loss-of-function model for dystrobrevin alpha. This polyclonal knockout cell pool provides a heterogeneous representation of gene-edited cells suitable for studying DTNA-dependent processes without clonal selection artifacts. The targeted gene disruption abrogates expression of the scaffolding protein dystrobrevin alpha, enabling functional interrogation of its role in cell adhesion and cytoskeletal organization.
The MES-OV host cell line is a mesenchymal ovarian cancer model established from high-grade serous ovarian carcinoma. It exhibits molecular features of the mesenchymal subtype, characterized by enhanced migratory and invasive properties. This cell line endogenously expresses components of the dystrophin-glycoprotein complex (DGC) and relies on integrin-mediated adhesion to the extracellular matrix, making it a physiologically relevant background for investigating DTNA function in ovarian tumor cell biology.
DTNA encodes dystrobrevin alpha, a key scaffolding protein within the dystrophin-glycoprotein complex (DGC). It interacts directly with dystrophin, utrophin, alpha-syntrophin, and beta-dystrobrevin to bridge the DGC to the actin cytoskeleton and downstream signaling effectors. Upstream, DTNA engagement is regulated by integrin-mediated adhesion and extracellular matrix components. Downstream, dystrobrevin alpha mediates signaling to neuronal nitric oxide synthase (nNOS), stabilizes the cortical actin network, and organizes cell-matrix adhesion complexes. Through these interactions, DTNA coordinates cytoskeletal dynamics and signal transduction critical for cell shape, adhesion, and mechanotransduction.
In the MES-OV mesenchymal ovarian cancer context, CRISPR/Cas9-mediated knockout of DTNA disrupts the structural and signaling integrity of the DGC. Loss of dystrobrevin alpha impairs anchorage of the DGC to the actin cytoskeleton, altering cell adhesion strength and cytoskeletal reorganization. Consequently, MES-OV DTNA knockout cells are expected to exhibit modified migration and invasion behaviors, providing a physiologically relevant platform to dissect the contribution of dystrobrevin alpha to ovarian cancer progression, particularly within the tumor microenvironment where matrix interactions drive metastasis.
These polyclonal knockout cells are ideally suited for a range of ovarian cancer research applications, including cell adhesion and migration assays, tumor microenvironment interaction studies, and cytoskeletal dynamics analysis. Typical experimental readouts include western blotting for dystrobrevin alpha and associated DGC proteins, immunofluorescence localization of adhesion complexes, transwell migration assays, quantitative cell adhesion assays, and RT-qPCR profiling of pathway components. Researchers can employ this model to investigate how DTNA loss influences ovarian cancer cell behavior and signaling. For additional technical information, please contact Ascent Research.
