The DVL3 Knockout MES-OV Polyclonal Cells constitute a CRISPR/Cas9-engineered polyclonal knockout population with targeted disruption of the DVL3 gene in the human ovarian clear cell carcinoma cell line MES-OV. As a polyclonal product, it contains a mixture of edited cells with diverse genetic modifications, offering a robust tool for functional genomics without the need for single-cell cloning. This format reduces clonal selection bias and maintains cellular heterogeneity, making it suitable for reproducible phenotypic assays.
MES-OV is a well-established human ovarian clear cell carcinoma cell line, characterized by clear cytoplasmic histology and aggressive tumor behavior. This model retains hallmarks of ovarian clear cell carcinoma, including altered signal transduction pathways that drive proliferation, survival, and metastasis. It serves as a valuable platform for dissecting the molecular basis of this chemoresistant cancer subtype and for evaluating targeted therapeutics.
DVL3 is a central phosphoprotein in WNT signal transduction, operating downstream of Frizzled receptors. In the canonical branch, DVL3 interacts with AXIN, APC, GSK3??, and CK1?? to block ??-catenin degradation, leading to nuclear ??-catenin/TCF4-mediated transcription of MYC and CCND1. In non-canonical pathways, DVL3 activates RAC1 and JNK via DAAM1 to regulate cell polarity and migration. Ligands such as WNT3A and WNT5A, together with co-receptors LRP5/6, trigger these cascades.
In the context of ovarian clear cell carcinoma, aberrant WNT/??-catenin signaling has been implicated in tumorigenesis, chemoresistance, and metastatic dissemination. DVL3 knockout in MES-OV cells enables dissection of its specific contributions to ovarian cancer phenotypes, including growth factor-independent proliferation, anoikis resistance, and invasive potential. This model is particularly relevant for understanding the molecular underpinnings of clear cell carcinoma and identifying vulnerabilities that can be exploited therapeutically.
These knockout cells are optimized for a range of applications in cancer research and drug discovery. They support WNT pathway interrogation using TOPFlash reporter assays, quantitative gene expression analysis by RT-qPCR, and protein-level validation via Western blotting. Functional studies such as cell migration and invasion transwell assays, immunofluorescence localization of WNT effectors, and phospho-signaling analysis of JNK and other kinases are readily performed. The model is suited for target validation in ovarian cancer and for screening inhibitors targeting DVL3 or downstream nodes. For further information, please contact Ascent Research.
