The DNMBP Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian carcinoma epithelial cell line. This polyclonal pool harbors targeted disruption of the DNMBP gene, eliminating functional DNMBP protein expression without clonal isolation. The heterogeneous knockout population allows researchers to study gene function while mitigating clonal artifacts, providing a robust loss-of-function model for investigating DNMBP??s roles in epithelial biology and ovarian cancer pathophysiology.
The parental MES-OV cell line is an established model of human high-grade serous ovarian carcinoma, retaining epithelial characteristics including cell?Ccell adhesion and junctional complexes. Derived from ovarian carcinoma tissue, MES-OV cells exhibit strong tumorigenic properties and are widely used in cancer research to examine mechanisms of epithelial-to-mesenchymal transition (EMT), invasion, and therapeutic resistance. Their epithelial phenotype makes them particularly suitable for dissecting the molecular basis of cell polarity and barrier function, which are often disrupted in malignancy.
DNMBP acts as a multidomain scaffold and guanine nucleotide exchange factor (GEF) for the small GTPase CDC42. Upon cell?Ccell contact, DNMBP is recruited to nascent adherens junctions via E-cadherin?Cmediated signals and activates CDC42. GTP-bound CDC42 then coordinates actin polymerization through downstream effectors including WASP and the ARP2/3 complex, promoting the assembly of cortical actin belts that stabilize tight and adherens junctions. DNMBP directly interacts with Dynamin-2 and ZO-1, linking endocytic machinery to junctional complexes. This signaling module integrates inputs from TGF??? receptors and RHOA, and further controls PAK1 and PAR6-based polarity pathways, ensuring proper epithelial architecture.
Loss of DNMBP function in ovarian carcinoma cells is associated with compromised junctional integrity, disrupted epithelial polarity, and enhanced migratory and invasive behavior??hallmarks of metastatic progression. By generating a polyclonal DNMBP knockout in the MES-OV background, researchers can interrogate how DNMBP deficiency alters tight junction protein localization, actin cytoskeleton dynamics, and CDC42?dependent signaling in a disease-relevant context. This model is highly pertinent for studying epithelial barrier dysfunction, early steps of metastasis, and the molecular interplay between oncogenic signaling and cell?Ccell adhesion pathways in ovarian cancer.
These knockout cells enable a wide range of downstream functional analyses. Typical applications include western blotting to verify loss of DNMBP and assess phosphorylation of CDC42 pathway components such as PAK1, immunofluorescence microscopy to examine ZO?1 and E?cadherin distribution, and RT?qPCR profiling of EMT markers. Functional assays may comprise transwell migration and invasion, real-time barrier integrity measurements via transepithelial electrical resistance (TEER), and Rho GTPase activation pull-downs. Furthermore, the cells can be used in drug screens to identify compounds that restore or mimic DNMBP?dependent junction stabilization. For detailed technical information or ordering, please contact Ascent Research.
