The CCNYL1 Knockout SK-HEP-1 Polyclonal Cells product consists of a heterogeneous population of SK-HEP-1 cells subjected to CRISPR/Cas9-mediated disruption of the CCNYL1 gene. As a polyclonal knockout collection, this model provides a representative loss-of-function background without clonal selection, enabling robust population-level analyses. The disruption targets the cyclin Y-like 1 locus, abrogating expression of the CCNYL1 protein and thereby eliminating its regulatory function in ??-catenin-dependent signaling cascades. This knockout model is supplied as a ready-to-use polyclonal cell stock suitable for comparative studies alongside parental SK-HEP-1 cells.
The SK-HEP-1 host cell line was originally derived from the ascitic fluid of a patient with liver adenocarcinoma and is widely employed as an in vitro model of hepatocellular carcinoma (HCC). Although its precise tissue origin remains debated??some studies suggest an endothelial rather than hepatic lineage??SK-HEP-1 cells reliably exhibit mesenchymal characteristics and a highly invasive phenotype. These features make them particularly valuable for investigating epithelial-mesenchymal transition (EMT) programs and metastatic dissemination in liver cancer. The cells are adherent, harbor wild-type TP53, and grow as a monolayer, facilitating a range of standard cell-based assays.
At the molecular level, CCNYL1 encodes a cyclin family protein that positively regulates the Wnt/??-catenin pathway. It forms a complex with the cyclin-dependent kinase CDK14 and is recruited to the LRP6 co-receptor upon WNT3A stimulation. The CCNYL1?CCDK14 complex phosphorylates LRP6, amplifying downstream signaling, inhibiting the AXIN?CGSK3?? destruction complex, and stabilizing cytosolic ??-catenin. Stabilized ??-catenin translocates to the nucleus, interacts with TCF/LEF transcription factors, and drives expression of proliferation genes including MYC and CCND1. Upstream regulators such as SOX2 and E2F modulate CCNYL1 expression.
In the context of SK-HEP-1 liver adenocarcinoma cells, disruption of CCNYL1 abrogates a critical node in Wnt/??-catenin signaling that is frequently hyperactivated in HCC. Given the mesenchymal and invasive properties of this cell line, CCNYL1 knockout provides a physiologically relevant system to dissect the contribution of Wnt-driven transcription to tumor cell migration, invasion, and metastatic potential. This polyclonal knockout population is particularly suited for experiments aimed at distinguishing canonical Wnt-dependent from non-canonical Wnt-related phenotypes, as well as for investigating crosstalk with other oncogenic pathways commonly deregulated in liver cancer.
Researchers can apply this knockout model to mechanistic studies of liver cancer biology, including Wnt pathway dissection, drug target validation, and functional analysis of proliferation and migration. Representative assays compatible with this model include western blotting for CCNYL1, CDK14, and ??-catenin; RT-qPCR quantification of MYC and CCND1 transcripts; TOP/FOP flash luciferase reporter assays; MTT viability measurements; Transwell migration and invasion assays; co-immunoprecipitation; flow cytometric cell cycle analysis; and immunofluorescence microscopy for ??-catenin localization. For technical inquiries or ordering, please contact Ascent Research.
