The DVL2 Knockout MES-OV Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population derived from the MES-OV human ovarian carcinoma cell line, in which the DVL2 gene has been disrupted. This polyclonal knockout product offers a pooled population of cells with heterogeneous gene editing events, enabling robust loss-of-function studies while mitigating clone-specific artifacts. The engineered cells provide a valuable tool for dissecting DVL2-dependent signaling mechanisms in an ovarian cancer context, without the influence of a single clonal background. The polyclonal nature ensures that observed phenotypes reflect target-gene disruption across a diverse genetic landscape, making it suitable for population-level functional assays and drug response screens.
The host MES-OV cell line is a well-characterized human ovarian carcinoma model, originally established from a patient tumor, and widely used to study the molecular underpinnings of epithelial ovarian cancer. These cells exhibit key features of ovarian cancer, including aberrant signaling pathways and altered proliferative control. MES-OV cells are particularly suited for investigating Wnt pathway deregulation, as they harbor active Wnt signaling components and respond to autocrine and paracrine Wnt cues. By introducing a DVL2 knockout in this background, researchers can directly assess the contribution of DVL2 to ovarian cancer cell behavior, including proliferation, migration, and chemoresistance, in a physiologically relevant cell context.
DVL2 (Dishevelled 2) is a cytoplasmic phosphoprotein that transduces Wnt signals from Frizzled receptors. In the canonical pathway, Wnt ligands (e.g., WNT3A, WNT5A) engage Frizzled (e.g., FZD7) and LRP5/6, recruiting DVL2 to the membrane where it interacts with AXIN1 and GSK3?? to inhibit the ??-catenin destruction complex. This stabilizes ??-catenin, enabling TCF/LEF-mediated transcription of targets such as AXIN2, MYC, and CCND1. DVL2 also activates non-canonical cascades: the PCP pathway via RHOA and RAC1, and the Ca2+ pathway through JNK. Phosphorylation by CK1?? and interaction with DIXDC1 further regulate DVL2 activity. Disruption of DVL2 thus attenuates both canonical and non-canonical Wnt signaling.
In ovarian carcinoma, DVL2 overexpression is associated with tumor progression, metastasis, and chemoresistance. DVL2 promotes proliferation and survival via ??-catenin-driven oncogene expression and enhances migration through RAC1/JNK pathways. Knockout in MES-OV cells enables dissection of these mechanisms and evaluation of Wnt inhibitor efficacy in a DVL2-deficient context.
This polyclonal knockout population supports Western blotting for DVL2 and ??-catenin, TOP/FOP Flash assays for TCF/LEF activity, immunofluorescence of ??-catenin localization, and RT-qPCR of target genes (AXIN2, MYC, CCND1). Phenotypic assays for proliferation, migration, and invasion are readily performed. Co-immunoprecipitation can probe DVL2 interactors. For inquiries, contact Ascent Research.
