CCDC117 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population derived from HeLa cells, designed to disrupt the endogenous CCDC117 gene. This polyclonal pool provides a heterogeneous loss-of-function model, enabling robust and reproducible studies of CCDC117-dependent processes without the need for single-cell cloning. The gene-edited cells are produced using a validated CRISPR/Cas9 system to target CCDC117, offering researchers a reliable tool for investigating centrosome biology and associated cellular pathways.
The host cell line, HeLa, is an immortalized epithelial cell line originally isolated from a cervical adenocarcinoma and is positive for human papillomavirus type 18 (HPV18). HeLa cells are among the most widely used models in cancer research due to their rapid proliferation and well-characterized genomic and transcriptomic landscapes. Their epithelial origin and transformed phenotype make them particularly suitable for examining cell cycle regulation, centrosome abnormalities, and mechanisms of genomic instability that underpin cervical and other solid tumors.
The CCDC117 gene encodes a coiled-coil domain-containing protein that localizes to centrosomes and plays a role in microtubule organization and centrosome maturation. At the molecular level, CCDC117 interacts with centriolar proteins CEP135 and CEP250, forming complexes that are critical for centrosome duplication and spindle pole integrity. Its expression is potentially regulated by E2F transcription factors, linking it to cell cycle control. Within the centrosome duplication pathway, CCDC117 functions upstream of or in concert with polo-like kinase 4 (PLK4) and cyclin-dependent kinase 1 (CDK1). Disruption of CCDC117 via CRISPR/Cas9 can impair proper spindle formation, leading to chromosome segregation errors, activation of DNA damage response, and increased genomic instability.
In the context of HeLa cervical cancer cells, the loss of CCDC117 is particularly informative because these cells already harbor p53 and Rb pathway inactivation due to HPV18 oncoproteins, making them prone to centrosome amplification and mitotic defects. Therefore, this knockout model amplifies the cellular phenotypes already observed in cancer, providing a sensitive platform to study centrosome dysfunction, aberrant cell cycle progression, and the resulting DNA damage. It serves as a potent tool for dissecting the interplay between viral oncogenesis and centrosome homeostasis.
Research applications for this product are extensive. Investigators can employ immunofluorescence microscopy to assess centrosome number and structure using antibodies against ??-tubulin or CEP135, and analyze spindle morphology. Western blotting of cell cycle regulators (e.g., Cyclin B1, CDK1) and flow cytometric DNA content analysis can reveal cell cycle perturbations. Proliferation assays (MTT) and DNA damage response markers such as ??H2AX foci formation can quantify functional consequences of CCDC117 loss. These tools support studies in centrosome biology, cancer cell cycle analysis, and genomic instability. For additional information or custom inquiries, please contact Ascent Research.
