The CCDC167 Knockout HeLa Polyclonal Cells product consists of a heterogeneous population of HeLa cells that have undergone CRISPR/Cas9-mediated disruption of the CCDC167 gene. This polyclonal knockout format preserves a diverse repertoire of loss-of-function mutations across the cell pool, offering a robust model for studying gene function without clonal selection artifacts. The engineered population is suitable for assays that require consistent target gene depletion while retaining some biological variability characteristic of mixed edited populations. Researchers can utilize this model to examine the consequences of CCDC167 loss in a human epithelial cancer context without imposing monoclonal biases in downstream analyses.
The host HeLa cell line is an HPV-positive cervical adenocarcinoma epithelial cell line extensively employed in biomedical research. These adherent cells retain key epithelial characteristics and, importantly, retain the capacity to assemble primary cilia upon serum starvation, making them a relevant system for ciliogenesis studies. Their rapid proliferation, genetic tractability, and well-characterized signaling landscape facilitate experiments requiring robust, reproducible readouts. The HPV-transformed background additionally permits investigation of potential crosstalk between viral oncoproteins and ciliary signaling pathways, offering a unique angle for exploring cancer cell biology.
CCDC167 encodes a centriolar satellite protein that functions at the interface between microtubule organization and primary cilium assembly. It physically interacts with PCM1 and CEP290, two core satellite components, to facilitate microtubule anchoring at the centrosome. Loss of CCDC167 disrupts centriolar satellite integrity, impairing the recruitment of ciliary machinery and ultimately dampening ciliogenesis. This defect propagates downstream to attenuate hedgehog signaling, as evidenced by reduced activation of GLI transcription factors, including GLI1, and diminished expression of hedgehog target genes. Key pathway nodes such as SMO, ARL13B, and INVS further relay signals across the cilium, and their functional engagement is compromised in the absence of CCDC167.
In the HeLa cell context, CCDC167 knockout provides a powerful tool to dissect cilia-dependent and independent roles of centriolar satellites in cancer-relevant phenotypes. Given that aberrant hedgehog signaling is linked to cervical cancer progression and HPV-mediated transformation, this model enables systematic exploration of how ciliary protein networks influence oncogenic processes. Moreover, the HeLa system??s compatibility with high-content imaging, drug treatments, and molecular perturbations makes it suitable for identifying chemical modulators of ciliogenesis and for interrogating the interplay between cilia dysfunction and epithelial tumor biology.
Typical applications include detailed characterization of ciliogenesis mechanisms using serum-starvation-induced ciliogenesis assays followed by immunofluorescence staining for ciliary markers such as ARL13B and acetylated tubulin. Researchers can also monitor hedgehog pathway activity via western blotting for GLI1 or RT-qPCR analysis of ciliary gene expression. Co-immunoprecipitation experiments enable verification of disrupted PCM1?CCCDC167 interactions, while functional rescue studies may elucidate structure?Cfunction relationships. The polyclonal pool is suited for drug screening campaigns targeting cilia-related disorders, ciliopathy disease modeling, and cancer cell biology investigations. For further information, please contact Ascent Research.
