The CCDC138 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, offering a gene-disrupted model in the widely utilized HeLa cervical adenocarcinoma epithelial cell line. This product enables loss-of-function studies of CCDC138 through CRISPR/Cas9-mediated target-gene disruption, generating a heterogeneous pool of knockout cells that preserves natural editing diversity and avoids clonal artifacts.
HeLa cells, isolated from a cervical adenocarcinoma, harbor integrated HPV18 sequences that inactivate p53 and Rb tumor suppressors, creating an immortalized epithelial model with robust growth kinetics. This background is extensively used in cell cycle, cancer biology, and centrosome research, providing a well-characterized platform for interrogating genes involved in microtubule organization and genomic stability.
CCDC138 encodes a coiled-coil domain protein implicated in centrosomal and ciliary functions. Its expression is regulated by FOXJ1, a master ciliogenic transcription factor, and by cyclin-dependent kinases in a cell cycle-dependent manner. At the centrosome, CCDC138 interacts with key structural proteins CEP135 and pericentrin, and is associated with ??-tubulin and microtubule motor proteins, suggesting a scaffold role in microtubule nucleation and anchoring. By recruiting microtubule-associated proteins (MAPs), CCDC138 influences microtubule dynamics and mitotic spindle assembly, with its disruption predicted to impair centrosome duplication and cilium formation.
In HeLa cells, HPV18-mediated disruption of p53 and Rb pathways leads to supernumerary centrosomes and genomic instability. Knocking out CCDC138 in this sensitized background can reveal its contribution to centrosome homeostasis and mitotic fidelity, aiding in the discrimination of tumor-suppressive versus oncogenic roles in cervical adenocarcinoma. The polyclonal pool allows assessment of population-level phenotypes such as centrosome amplification, multipolar spindles, and defective ciliogenesis.
Key applications include immunofluorescence imaging for centrosomal markers (pericentrin, CEP135, ??-tubulin), microtubule regrowth assays to evaluate nucleation, and co-immunoprecipitation to validate candidate interactions. Cell cycle analysis by flow cytometry and serum starvation-induced ciliogenesis assays further enable functional characterization. These knockout cells provide a versatile system for centrosome biology, ciliogenesis, and cancer research. For technical support and additional product information, please contact Ascent Research.
