The CCDC127 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of human MES-OV ovarian carcinoma cells designed for loss-of-function studies of the CCDC127 gene. This polyclonal format preserves genetic heterogeneity, making it suitable for population-based assays and pooled functional screens where clonal artifacts are minimized. The disruption of CCDC127 is achieved through CRISPR/Cas9-mediated gene targeting, providing a robust model for investigating centrosome biology and mitotic regulation.
The host MES-OV cell line, derived from human ovarian adenocarcinoma, exhibits a mesenchymal phenotype characteristic of the aggressive mesenchymal subtype of ovarian cancer. These cells display enhanced migratory and invasive properties, offering a relevant model for studying tumor dissemination. Editing in this background allows dissection of pathways linking centrosome function to mesenchymal features and therapeutic response.
CCDC127 is a centrosomal protein essential for microtubule organization and mitotic spindle assembly. It is phosphorylated by the master mitotic kinases PLK1 and Aurora A, and interacts with pericentriolar components including PCM1, CEP family proteins, and tubulin subunits. These interactions mediate the recruitment of gamma-tubulin to centrosomes, promoting microtubule nucleation and subsequent mitotic progression. Thus, CCDC127 functions downstream of CDK1, PLK1, and Aurora A, integrating kinase signals to ensure centrosome maturation and bipolar spindle formation.
In the MES-OV ovarian carcinoma model, CCDC127 knockout disrupts centrosome-mediated microtubule organization, potentially leading to mitotic errors, chromosomal instability, and altered sensitivity to microtubule-targeting chemotherapeutics. This model enables investigation of centrosome dysfunction in the context of mesenchymal ovarian cancer, a subtype associated with poor prognosis. Researchers can study how loss of CCDC127 influences tumor cell migration, invasion, and drug response, contributing to the understanding of centrosome-related oncogenic mechanisms.
Common applications include immunofluorescence staining of centrosomal markers (gamma-tubulin, pericentrin), western blot analysis of mitotic regulators (e.g., phospho-Aurora A, cyclin B1), cell cycle profiling by flow cytometry, cell viability and migration assays, and transcriptomic analysis via RNA-seq. The polyclonal knockout population is also amenable to pooled CRISPR screens for synthetic lethality or drug modifier studies. This CCDC127-deficient MES-OV cell product is a valuable tool for centrosome research, mitotic kinase signaling, and ovarian cancer biology. For inquiries, please contact Ascent Research.
