The CCNY Knockout SK-HEP-1 Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human SK-HEP-1 hepatocellular carcinoma line. This product offers a heterogeneous pool of CCNY-disrupted cells, serving as a loss-of-function model to study cyclin Y in its native genomic context. The polyclonal format minimizes clonal artifacts and enables robust analysis of gene function at the population level.
SK-HEP-1 is a human epithelial cell line originally isolated from a liver adenocarcinoma. These adherent, tumorigenic cells are widely used as a model for hepatocellular carcinoma (HCC), providing a relevant system for investigating liver cancer biology, drug metabolism, and metastatic behavior.
CCNY encodes cyclin Y, an essential activator of CDK14 and CDK16. Within the Wnt/??-catenin pathway, Wnt3a ligand engagement of Frizzled receptors and LRP6 co-receptor triggers recruitment of DVL2 and the CCNY?CCDK14/CDK16 complexes. This promotes CDK14/CDK16-mediated LRP6 phosphorylation, leading to ??-catenin stabilization and nuclear translocation. ??-Catenin subsequently complexes with TCF/LEF transcription factors to drive expression of cell cycle regulators such as MYC, CCND1, and AXIN2. Thus, CCNY links extracellular Wnt3a signals to the G1/S transition and proliferative gene programs.
Disruption of CCNY in SK-HEP-1 cells abolishes CDK14/CDK16-dependent LRP6 phosphorylation, crippling Wnt/??-catenin signal transduction and reducing transcription of pro-proliferative target genes. This manifests as impaired cell proliferation, reduced colony formation, and cell cycle defects, underscoring the role of cyclin Y in HCC tumor properties. The model is therefore ideal for dissecting Wnt-dependent oncogenic mechanisms in liver cancer.
Researchers can deploy this knockout model for detailed Wnt signaling analyses using TopFlash luciferase reporter assays and Western blotting for ??-catenin and downstream targets. Functional assays including cell proliferation, colony formation, flow cytometric cell cycle analysis, and migration studies enable comprehensive phenotypic characterization. Transcriptomic approaches such as RNA-seq further allow global mapping of CCNY-dependent pathways. These polyclonal knockout cells support drug target validation and cell cycle research in an HCC context. For inquiries, please contact Ascent Research.
