DST Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the DST gene in the A2780 human ovarian carcinoma cell line. This heterogeneous pool of gene-disrupted cells provides a robust loss-of-function model for studying DST-dependent processes without the biases of clonal selection. The product is designed for investigations into cytoskeletal organization, cell adhesion, and related signaling in an epithelial cancer setting.
The parental A2780 line, derived from an untreated ovarian carcinoma patient, is a well-established model for epithelial ovarian cancer research. It retains key features including epithelial morphology, adhesion-dependency, and invasive capacity, making it widely used to study cancer biology, drug resistance, and metastasis.
DST encodes dystonin (BPAG1), a giant cytoskeletal linker protein that connects intermediate filaments, actin, and cell-matrix adhesion complexes. It interacts with keratins, actin, ITGB4, plectin, ERM proteins, BPAG2, and functions within complexes containing ITGA6/ITGB4, COL17A1, and laminin-332 to stabilize hemidesmosomes. Upstream, DST is regulated by TP63, mechanical stress, and integrin-mediated adhesion signals. Downstream, it organizes keratin intermediate filament networks and maintains focal adhesion integrity. Knockout of DST disrupts hemidesmosome assembly and intermediate filament organization, resulting in reduced cellular cohesion and adhesion. Clinically, DST mutations cause skin blistering disorders and neuropathies, reflecting its critical function in mechanical resilience.
In the A2780 ovarian carcinoma model, DST knockout provides a platform to dissect the role of cytoskeletal integrity in cancer cell behavior. Ovarian cancer dissemination involves peritoneal adhesion and migration under mechanical stress, processes that depend on dynamic cell?Cmatrix interactions. DST deficiency may compromise the ability of A2780 cells to withstand these forces, impair migration, and alter metastatic potential. This model is thus valuable for identifying mechanosensitive signaling pathways and testing compounds that target structural vulnerabilities in cancer cells.
This knockout cell population is suitable for western blotting, RT-qPCR, and immunofluorescence to confirm DST ablation and visualize cytoskeletal changes. Functional assays including adhesion, migration, and invasion experiments quantify altered cell?Cmatrix interactions, while atomic force microscopy measures mechanical properties. Drug sensitivity screens can identify compounds exploiting structural weaknesses. For further information or to order, please contact Ascent Research.
