The CCDC117 Knockout SK-HEP-1 Polyclonal Cells product is a heterogeneous pool of SK-HEP-1 cells harboring CRISPR/Cas9-mediated disruption of the CCDC117 gene, constituting a polyclonal knockout population. The polyclonal format bypasses single-cell cloning, preserving genetic heterogeneity while achieving collective target gene silencing and minimizing clonal adaptation artifacts. This ready-to-use population facilitates immediate downstream assays and is particularly suitable for pooled screening and population-level phenotypic analyses where clonal variation is undesirable.
The host cell line SK-HEP-1 is an immortalized human liver adenocarcinoma line isolated from the ascitic fluid of a hepatocellular carcinoma patient. These epithelial cancer cells retain key oncogenic properties and are widely employed as an in vitro model for studying hepatocarcinogenesis, tumor cell proliferation, and drug responses. Their adherent growth, robust proliferation, and well-documented molecular profile make them a practical and clinically relevant system for functional genomics investigations.
CCDC117 encodes a coiled-coil domain protein that functions as a critical regulator of centrosome duplication and mitotic progression. It operates within a signaling network involving upstream kinases CDK1 and PLK1, downstream effectors Cyclin B1 and CDC20, and direct interacting partners CEP63, CEP152, and CDK5RAP2. Through these associations, CCDC117 coordinates centriole biogenesis and spindle assembly; its disruption leads to centrosome defects, mitotic arrest, and impaired proliferation. The protein thus integrates centrosome cycle control with the cell cycle engine, ensuring accurate chromosome segregation.
In SK-HEP-1 hepatocellular carcinoma cells, CCDC117 knockout likely exposes cancer cell dependencies on proper centrosome function, especially given the frequent mitotic checkpoint dysregulation in tumors. This model enables dissection of centrosome-related mechanisms that may drive genomic instability and tumor evolution. It also offers a platform for identifying therapeutic vulnerabilities arising from centrosome stress and for validating drugs that target mitotic machinery, potentially guiding novel treatment strategies for liver cancer.
This polyclonal knockout tool supports diverse applications, including cancer cell proliferation studies, cell cycle regulation analyses, and centrosome biology research. Representative assays such as Western blotting for Cyclin B1 and phosphorylated histones, immunofluorescence staining of centrosomal components, colony formation, RT-qPCR, and phospho-histone H3 mitotic index determination can be readily performed. The population is also amenable to live-cell imaging of mitosis, flow cytometric cell cycle profiling, and functional genomics screens. It is an invaluable resource for academic and industry researchers investigating hepatocellular carcinoma and centrosome biology. For further inquiries, please contact Ascent Research.
