The CCNYL1 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian cancer cell line. These cells harbor a targeted disruption of the CCNYL1 gene, resulting in a loss-of-function model for studying Cyclin Y-like 1. The polyclonal format provides a mixed population of edited alleles, enabling robust functional studies without the clonal selection artifacts often associated with single-cell-derived knockouts. This product is designed for researchers investigating Wnt signaling, cell cycle regulation, and ovarian cancer biology.
MES-OV is a mesenchymal-type ovarian clear cell carcinoma cell line that faithfully recapitulates key features of human ovarian cancer. Established from a patient-derived tumor, this adherent line exhibits aggressive proliferation and migratory properties characteristic of the mesenchymal subtype. The MES-OV background provides a clinically relevant context for dissecting oncogenic signaling pathways, particularly those driving tumor progression and metastasis in ovarian carcinoma.
CCNYL1 encodes Cyclin Y-like 1, a cyclin partner that activates CDK14 kinase. Upon Wnt ligand stimulation, the CCNYL1?CCDK14 complex phosphorylates the Wnt co-receptor LRP6, triggering downstream signaling through DVL and the ??-catenin destruction complex. This leads to ??-catenin stabilization, nuclear translocation, and TCF/LEF-mediated transcription of target genes. CCNYL1 thus functions as a positive regulator of the Wnt/??-catenin pathway, linking extracellular Wnt signals to cell cycle progression and cytoskeletal dynamics. Interacting partners include CDK14, LRP6, and ??-catenin, while downstream effectors encompass TCF/LEF-dependent gene programs.
In MES-OV cells, CCNYL1-mediated enhancement of Wnt signaling is thought to drive proliferation and migration, processes essential for ovarian tumor growth and dissemination. By abolishing CCNYL1 expression, these polyclonal knockout cells enable direct assessment of CCNYL1’s contribution to oncogenic phenotypes. The polyclonal nature avoids potential genetic drift or compensatory mutations that can arise during clone selection, thereby preserving the biological variability of the original cell population and yielding results more representative of actual tumor heterogeneity.
Typical applications include investigating Wnt/??-catenin signal transduction by western blotting and phospho-LRP6 analysis, quantifying transcriptional responses via RT-qPCR and TOPFlash reporter assays, and evaluating functional impacts on proliferation and migration through established in vitro assays. Co-immunoprecipitation can verify CCNYL1?CCDK14 or CDK14?CLRP6 interactions. This knockout model is well-suited for drug target validation studies and for identifying synthetic lethal interactions in ovarian cancer. For further information, please contact Ascent Research.
