The CCNY Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of MES-OV human mesenchymal stem cells (MSCs) with targeted disruption of the cyclin Y (CCNY) gene. This heterogeneous model preserves the biological variability of primary MSC cultures and avoids clone-specific artifacts. The mixed knockout pool provides a robust loss-of-function system for functional studies in cancer and stem cell biology.
MES-OV cells are derived from human ovarian tissue and display hallmark mesenchymal stromal cell features: self-renewal, adherence-dependent growth, and multipotent differentiation into adipocytes, osteoblasts, and chondrocytes. They also possess tissue-regenerative and immunomodulatory capacities, making them a physiologically relevant model for studying signaling pathways governing stem cell maintenance, differentiation, and tumor-stroma interactions, particularly in ovarian cancer contexts.
CCNY forms a kinase complex with CDK14 that phosphorylates LRP6, enhancing Wnt/??-catenin signaling. This recruits DVL2 and inhibits the destruction complex (GSK3??, Axin, APC), stabilizing ??-catenin, which translocates to the nucleus and activates TCF/LEF-dependent transcription of MYC and CCND1. CCNY is regulated by ??-catenin/TCF and E2F, linking growth factor signals (EGF, FGF) to cell-cycle regulators Rb and CDK2 to drive G1/S progression.
In MES-OV MSCs, CCNY disruption enables dissection of Wnt-driven proliferation and differentiation control. Given CCNY overexpression in multiple carcinomas (breast, gastric, lung, ovarian, colorectal) and the ovarian origin of the host cells, this model is particularly suited for ovarian cancer research. Knockout cells can reveal CCNY’s role in stromal cell quiescence, self-renewal, and lineage commitment, as well as its contribution to tumor microenvironment signaling and drug resistance.
Research applications include in-depth analysis of Wnt/??-catenin signaling, cell-cycle regulation, and oncogenic mechanisms in breast, gastric, lung, ovarian, and colorectal cancer models. The polyclonal knockout format is compatible with population-based functional assays such as MTT and BrdU proliferation measurements, flow cytometric cell-cycle phase distribution, transwell migration and Matrigel invasion assays, and quantitative real-time PCR for Wnt transcriptional targets like MYC and CCND1. Protein-level validation can be performed via Western blotting for ??-catenin, phospho-LRP6, and downstream effectors, while TOP/FOPflash dual-luciferase reporters quantify ??-catenin transcriptional activity. Drug response studies using Wnt pathway inhibitors (e.g., XAV939, IWP-2) can identify CCNY-dependent therapeutic vulnerabilities. For experimental guidance or product inquiries, please contact Ascent Research.
