The CCNYL1 Knockout Huh-7 Polyclonal Cells from Ascent Research are a CRISPR/Cas9-edited polyclonal knockout population of human Huh-7 hepatocellular carcinoma cells with targeted disruption of the CCNYL1 locus. This polyclonal format retains genetic heterogeneity from the editing process, offering a representative loss-of-function model for studying cyclin Y-like 1 function without clonal selection.
Huh-7 is a well-differentiated hepatocellular carcinoma cell line derived from a liver tumor in a 57-year-old Japanese male. It exhibits adherent, epithelial morphology and serves as a widely used model for hepatic metabolism, liver cancer biology, and hepatocarcinogenesis, owing to its faithful retention of hepatocyte-specific functions and robust tumorigenic properties.
CCNYL1 encodes a regulatory subunit of the cyclin-dependent kinase 11 (CDK11) complex that governs pre-mRNA splicing and transcription. CCNYL1 forms complexes with CDK11 and spliceosome core components including SF3B1, PRPF8, and U2 snRNP to modulate splice site selection and processing efficiency. Disruption of CCNYL1 impairs the CDK11-cyclin Y-like 1 holoenzyme, leading to aberrant splicing of downstream targets such as the CCND1 cell cycle regulator and apoptosis-related transcripts. These splicing alterations are propagated by upstream signals that direct spliceosome assembly and CDK11 activation.
In Huh-7 liver cancer cells, loss of CCNYL1 disrupts splicing networks essential for tumor cell proliferation and survival. The polyclonal knockout model enables examination of global splicing dysregulation and its phenotypic consequences, including changes in cell growth, apoptotic balance, and response to spliceosome-targeted inhibitors. This system is particularly relevant for dissecting splicing-dependent mechanisms in hepatocellular carcinoma, a disease where aberrant mRNA processing frequently drives oncogenesis and therapeutic resistance.
Key applications include functional characterization of CCNYL1 in liver cancer, validation of spliceosome inhibitors as therapeutic candidates, and mechanistic studies of RNA processing in oncogenic settings. Typical assays involve RT-PCR and RNA-seq for splicing variant analysis, western blot and co-immunoprecipitation for CDK11 complex integrity, and cell-based proliferation and apoptosis assays. Together, this polyclonal knockout model provides a versatile platform for both fundamental and translational liver cancer research. Researchers seeking additional details or support are encouraged to contact Ascent Research.
