The CCDC102A Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population with targeted disruption of the CCDC102A gene in the human SK-HEP-1 hepatocellular carcinoma cell line. This loss-of-function model enables study of CCDC102A, a coiled-coil domain protein linked to centrosome duplication, ciliary assembly, and cytoskeletal organization. The polyclonal format retains genetic diversity, avoiding clonal selection artifacts.
SK-HEP-1 cells were derived from ascitic fluid of a male patient with liver adenocarcinoma and display mixed hepatocytic and endothelial features. This unique phenotype makes them a reliable model for liver cancer research, tumor angiogenesis, and studies of epithelial?Cmesenchymal plasticity. Their dual character allows investigation of centrosome and ciliary functions in both carcinoma cell growth and angiogenic behavior.
CCDC102A is a predicted coiled-coil scaffold protein at the centrosome and ciliary base. Its expression is regulated by E2F transcription factors and FOXJ1, and it interacts with centriolar proteins such as CPAP/CENPJ and tubulin. Downstream, CCDC102A converges on centrosome integrity regulators like PLK4 and SAS6, and ciliary transport components IFT88 and ARL13B. Mechanistically, CCDC102A coordinates centriole duplication and cilia assembly; its disruption impairs centrosome maturation and primary cilia formation.
In hepatocellular carcinoma, centrosome abnormalities and ciliary defects contribute to genomic instability and altered signaling. SK-HEP-1 CCDC102A knockout cells provide a relevant system to dissect these processes. Loss of CCDC102A may induce centriole overduplication and ciliary dysfunction, affecting proliferation, migration, and angiogenic potential. This polyclonal model is therefore valuable for bridging centrosome biology and liver cancer pathology.
This knockout cell population is compatible with immunofluorescence for centrosome markers (??-tubulin, centrin), cilia formation assays, cell cycle analysis, western blotting, and functional assays for proliferation, migration, and invasion. RNA-seq can further profile transcriptomic changes. It is ideal for functional genomics, drug discovery targeting centrosome and cilia pathways, and mechanistic studies in hepatocellular carcinoma. For further information, contact Ascent Research.
