CCDC82 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in the HeLa human cervical adenocarcinoma cell line, designed for loss-of-function studies of the CCDC82 gene. This product offers a heterogeneous pool of cells with targeted gene disruptions, avoiding the clonal selection artifacts of monoclonal lines and providing a robust system for examining CCDC82-dependent mechanisms in centriolar satellite organization, ciliogenesis, and associated signaling pathways.
HeLa cells are an epithelial line derived from cervical adenocarcinoma, characterized by HPV-18 positivity and inactivation of the p53 and Rb tumor suppressors. This genetic profile confers a highly proliferative phenotype and has established HeLa as a widely used model in cancer biology, cell cycle research, and microtubule dynamics studies. The host background provides a well-defined context for exploring the interplay between oncogenic signaling and cilia-related processes.
CCDC82 is a centriolar satellite protein that interacts physically with PCM1, CEP131, and CEP290 to coordinate the delivery of ciliary components essential for primary cilium assembly. Its function is influenced by cell cycle-dependent kinases including PLK1, and it acts upstream of Hedgehog signaling effectors such as GLI transcription factors. Disruption of CCDC82 compromises centriolar satellite organization, leading to impaired ciliogenesis and attenuated Hedgehog pathway activity, thereby linking centrosome cycle control to cilia-dependent signaling in both normal and disease states.
In the HeLa cervical adenocarcinoma background, where p53 and Rb are inactivated, loss of CCDC82 offers a unique opportunity to examine centriolar satellite function in a hyperproliferative, transformed epithelial setting. The polyclonal knockout population allows assessment of ciliogenesis defects and Hedgehog signaling alterations without the confound of clonal variability. By disrupting CCDC82 in this widely used cancer cell line, researchers can explore the crosstalk between cell cycle progression, cilia dynamics, and oncogenic pathways, facilitating mechanistic studies relevant to ciliopathy-associated cancer phenotypes.
Typical experimental approaches include immunofluorescence detection of cilia markers Arl13b and acetylated tubulin following serum starvation-induced ciliogenesis, western blotting for PCM1 and CCDC82, and co-immunoprecipitation to probe centriolar satellite complex interactions. Additional applications encompass cell cycle analysis by flow cytometry, functional rescue experiments, and ciliogenesis assay development. This knockout model supports investigations into ciliopathies, centriolar satellite biology, and cancer cell proliferation. For further information and technical guidance, please contact Ascent Research.
