The DOCK7 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the mouse MES-OV ovarian surface epithelial carcinoma cell line. This product offers researchers a robust loss-of-function model to interrogate DOCK7 gene function in an ovarian cancer context. The polyclonal population carries heterogeneous CRISPR/Cas9-mediated disruptions at the DOCK7 locus, enabling assessment of gene ablation effects without the biases associated with single-cell cloning. The polyclonal format ensures representation of diverse editing events, facilitating population-level phenotypic analyses.
MES-OV is a well-characterized murine ovarian carcinoma cell line originating from ovarian surface epithelium, the presumed cell of origin for most epithelial ovarian cancers. These cells maintain an epithelial phenotype and are extensively used to model ovarian tumorigenesis, metastatic dissemination, and therapeutic response. As a model of ovarian surface epithelial carcinoma, MES-OV provides a physiologically relevant platform to investigate molecular drivers of ovarian cancer progression, particularly mechanisms governing migration, invasion, and epithelial-mesenchymal transition (EMT).
DOCK7 functions as a guanine nucleotide exchange factor (GEF) that specifically activates Rac1 and Cdc42 by catalyzing GDP-to-GTP exchange. Upstream signals such as Neuregulin-ErbB receptor engagement, Cdk5 kinase, or integrin activation stimulate DOCK7, leading to the generation of Rac1-GTP and Cdc42-GTP. These activated GTPases signal through PAK kinases, the WAVE complex, and Arp2/3 to promote actin polymerization and cytoskeletal reorganization. DOCK7 directly interacts with TACC3, and through the ErbB?CDOCK7?CRac1?CPAK?CWAVE?CArp2/3?Cactin pathway, it coordinates cell migration, neurite outgrowth, and Schwann cell myelination. In cancer, this pathway drives lamellipodia formation and focal adhesion dynamics essential for invasion.
In the MES-OV ovarian carcinoma background, DOCK7 knockout is anticipated to severely impair Rac1/Cdc42-driven actin polymerization, leading to diminished migratory and invasive capacities. Given DOCK7??s established role in metastasis and its link to developmental and epileptic encephalopathy, this model enables dissection of the cytoskeletal and signaling networks that underpin ovarian cancer dissemination. The polyclonal DOCK7 knockout cells are particularly valuable for exploring how DOCK7-dependent pathways influence EMT, matrix degradation, and transendothelial migration, all critical steps in the metastatic cascade.
Researchers can employ these DOCK7 knockout cells in wound healing and transwell migration assays to evaluate motility, phalloidin staining to assess actin reorganization, and Rac1/Cdc42 activation pull-downs to measure GTPase activity. The model also supports EMT analysis via western blotting and immunofluorescence, as well as drug sensitivity screens to identify compounds selectively affecting DOCK7-deficient cells. For further technical details or ordering, contact Ascent Research.
