CCDC171 Knockout HeLa Polyclonal Cells consist of a polyclonal population of HeLa cells that have undergone CRISPR/Cas9-mediated gene disruption at the CCDC171 locus. This product provides a loss-of-function model for the study of CCDC171, a coiled-coil domain-containing protein associated with centrosomal and ciliary functions. As a polyclonal knockout population, it offers a genetically diverse background that minimizes clonal selection bias, making it suitable for pooled functional assays and drug screening applications.
The host HeLa cell line is an immortalized epithelial cell line derived from a human cervical adenocarcinoma. HeLa cells are widely employed in cancer research due to their robust growth, tumorigenic properties, and well-characterized genome. Under conditions of serum deprivation, HeLa cells can be induced to assemble primary cilia, providing a tractable system for investigating ciliogenesis and ciliary signaling in a cervical cancer context. This feature, combined with their ease of genetic manipulation, makes HeLa an ideal platform for targeted gene knockout studies.
CCDC171 encodes a protein that localizes to the centrosome and basal body and is involved in centrosome maturation, primary cilium assembly, and Hedgehog signal transduction. It physically interacts with centrosomal components such as CEP120 and CEP164, as well as ciliary proteins including IFT88 and OFD1. The regulation of CCDC171 is controlled by RFX transcription factors and FOXJ1, while it functions genetically downstream of Hedgehog pathway effectors like GLI1 and GLI3. Disruption of CCDC171 leads to defects in primary cilium formation and attenuated Hedgehog signaling, highlighting its role in linking centrosome integrity to ciliary function and developmental signaling.
In HeLa cells, knockout of CCDC171 impairs ciliogenesis and disrupts centrosomal organization, offering a powerful model to study how ciliary defects contribute to cervical cancer cell behavior. Ciliary dysfunction is increasingly associated with cancer hallmarks such as aberrant migration, invasion, and dysregulated proliferation, and the CCDC171 knockout enables dissection of these processes in an epithelial tumor setting. Moreover, because HeLa cells express key Hedgehog pathway components, this model permits the investigation of crosstalk between ciliary assembly and Hedgehog signaling in a context relevant to cervical adenocarcinoma.
Researchers can utilize this polyclonal knockout population for immunofluorescence-based analysis of ciliary markers like acetylated tubulin and ARL13B, as well as centrosomal proteins pericentrin and ??-tubulin. Western blotting can assess Hedgehog pathway activation through GLI1 and GLI3 levels, while RT-qPCR quantifies changes in ciliary gene expression. The model is suitable for migration and invasion assays to evaluate CCDC171-dependent cell motility and for pooled validation of siRNA or shRNA-mediated CCDC171 knockdown. Additionally, these cells can be employed in high-throughput screening to identify compounds that modulate ciliogenesis or Hedgehog signaling, serving drug discovery efforts for ciliopathies and cervical cancer. For additional information, please contact Ascent Research.
