The CCDC71L Knockout SK-HEP-1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the CCDC71L gene has been disrupted to generate a loss-of-function model. This polyclonal format provides a heterogeneous pool of edited cells expressing a range of target-gene disruptions, enabling robust functional studies without the selective pressure of clonal expansion. The product is designed for researchers investigating the roles of the coiled-coil domain-containing protein CCDC71L in centrosome biology, ciliogenesis, and cell cycle control.
The host cell line SK-HEP-1 is a human hepatic adenocarcinoma cell line originally derived from a hepatocellular carcinoma patient. These cells exhibit a unique biphenotypic profile, displaying both epithelial and endothelial characteristics, and are widely used as a model for hepatocellular carcinoma and liver sinusoidal endothelial cells. This dual identity enables the study of tumor cell biology, angiogenesis, and endothelial?Cepithelial interactions within the hepatic microenvironment.
CCDC71L encodes a coiled-coil domain protein that is putatively involved in centrosome organization and primary cilia formation. It is transcriptionally regulated by E2F transcription factors and FOXM1, and functions downstream of these cell cycle regulators to modulate centrosomal protein dynamics. The protein interacts with key centrosomal components, including gamma-tubulin, pericentrin, and members of the CEP family. Within the centrosome duplication pathway, CCDC71L operates alongside CDK1, PLK4, and SAS-6, contributing to centriole assembly and mitotic spindle pole organization. Disruption of CCDC71L is predicted to perturb microtubule network integrity and downstream centrosomal protein localization.
In the context of SK-HEP-1 cells, CCDC71L knockout provides a physiologically relevant model to dissect the interplay between centrosome abnormalities, ciliogenesis defects, and liver cancer cell behavior. The loss of CCDC71L may lead to centrosome amplification, aberrant spindle orientation, and impaired primary cilium formation, which in turn can influence cell proliferation, migration, and signaling pathways associated with hepatocellular carcinoma. These polyclonal knockout cells are thus particularly suited for investigating the putative links between centrosomal dysfunction and hepatocarcinogenesis, as well as exploring ciliopathy-related phenotypes in a transformed hepatic background.
Researchers can employ this polyclonal knockout model in a wide range of experimental settings, including immunofluorescence-based analysis of centrosomal markers such as gamma-tubulin and pericentrin, flow cytometric cell cycle profiling, western blotting of centrosomal and cell cycle proteins, and cilia formation assays following serum starvation. Additional applications encompass migration and proliferation assays to assess functional outcomes of CCDC71L loss. The product is an essential tool for functional genomics of coiled-coil domain proteins and for advancing understanding of centrosome-related liver cancer biology. For detailed technical specifications and ordering information, please contact Ascent Research.
