The CCDC71 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population targeting the CCDC71 gene in the HeLa human cervical adenocarcinoma cell line. This product serves as a loss-of-function model for studying CCDC71, a coiled-coil domain-containing protein predicted to function in ciliogenesis and protein scaffolding. The polyclonal format yields a heterogeneous knockout pool, enabling population-level analyses while avoiding clonal artifacts. The CRISPR/Cas9-mediated gene disruption creates a versatile tool to dissect the poorly characterized roles of CCDC71. Researchers can employ these cells to investigate ciliary assembly and signaling in an immortalized epithelial context.
HeLa cells are an immortalized human cervical adenocarcinoma line originally derived from a patient??s tumor; they are HPV18-positive and exhibit robust epithelial morphology. This widely used cell line offers high transfectability and rapid proliferation, making it a staple in cancer biology and molecular cell research. While HeLa cells are not typically classified as ciliated under standard culture conditions, they retain the genetic machinery to assemble primary cilia upon serum deprivation or specific induction, rendering them suitable for ciliogenesis assays. Their cervical adenocarcinoma origin further positions them as a relevant model for studying oncogenic signaling pathways, including those modulated by ciliary proteins.
CCDC71 encodes a coiled-coil domain-containing protein predicted to localize to primary cilia, facilitating protein-protein interactions essential for ciliogenesis and Hedgehog signaling. It may scaffold components such as SMO and GLI transcription factors downstream of the Hedgehog pathway. Direct interactions remain unknown, but CCDC71 is predicted to associate with IFT particles and the BBSome complex, critical for ciliary trafficking. Upstream regulators may include ciliogenic transcription factors RFX and FOXJ1. Disruption of CCDC71 enables dissection of its contributions to cilia-dependent signaling and potential crosstalk with oncogenic pathways in cervical cancer.
In HeLa cells, CCDC71 knockout permits analysis of how loss of this ciliary scaffold affects cervical adenocarcinoma behavior. HeLa cells exhibit aberrant Hedgehog pathway activity that promotes proliferation and survival; deleting CCDC71 allows assessment of ciliary Hedgehog signaling and tumorigenic properties. The polyclonal population mirrors tumor microenvironment heterogeneity, enabling study of CCDC71??s role in cilia-related networks and their impact on cancer phenotypes. This model bridges ciliogenesis research and cervical cancer biology, offering a platform to elucidate ciliary dysfunction in oncogenesis.
Typical applications include ciliogenesis assays using serum starvation to induce cilia formation, followed by immunofluorescence microscopy to examine ciliary length and composition. Co-immunoprecipitation and western blotting can probe protein interactions and signaling changes, while RT-qPCR enables transcriptional profiling of Hedgehog target genes such as GLI1. Cell proliferation assays evaluate functional consequences on growth. The polyclonal nature of this knockout product is well suited for pooled screening approaches to identify genetic or pharmacological modifiers of CCDC71-dependent phenotypes. For additional information or to inquire about related products and custom services, please contact Ascent Research.
