The CCDC34 Knockout HeLa Polyclonal Cells represent a heterogeneous population of HeLa cells engineered via CRISPR/Cas9-mediated disruption of the CCDC34 gene locus. This polyclonal knockout model preserves a mixture of edited genotypes, reducing clonal artifacts and providing a robust loss-of-function system for studying CCDC34??s role in oncogenic signaling and proliferation. The product is generated using advanced CRISPR/Cas9 genome editing to introduce targeted gene disruption, enabling researchers to interrogate the functional consequences of CCDC34 loss in cancer-relevant contexts.
HeLa cells, a widely used cervical adenocarcinoma line, are HPV18-positive and aneuploid, displaying a transformed phenotype with rapid growth. These epithelial cells have been foundational in cancer research, including studies on viral oncogenesis, cell cycle control, and drug response. Their well-characterized molecular background and robust growth characteristics make them an optimal host for generating CRISPR knockouts to investigate tumor-associated genes and oncogenic pathways.
CCDC34, a coiled-coil domain-containing protein, promotes cell proliferation and tumorigenesis. It operates downstream of transcription factors MYC and E2F1 and is linked to the MAPK/ERK and PI3K/AKT pathways. Disruption of CCDC34 is expected to downregulate key effectors such as CCND1, CDK4, PCNA, and MKI67, consequently impairing cell cycle progression. Although its direct interactors are uncharacterized, predicted cytoskeletal associations via its coiled-coil domain may contribute to its mitogenic functions. Representative pathway components MAPK1/3, AKT1, CCND1, CDK4, and PCNA mediate the signaling networks affected by CCDC34 loss, underscoring its integration into critical oncogenic cascades.
In HeLa cells, where HPV oncoproteins already dysregulate p53 and Rb, CCDC34 knockout is predicted to further attenuate proliferative and tumorigenic capacity by disrupting downstream oncogenic signals. This model allows dissection of CCDC34-dependent mechanisms that collaborate with viral transformation, potentially revealing therapeutic vulnerabilities. By using this system, researchers can explore how CCDC34 cooperates with HPV-mediated oncogenesis and test inhibitors targeting downstream effectors. The polyclonal nature better reflects tumor heterogeneity, enhancing translational research value and reducing the risk of clonal selection bias.
This product is suited for oncogene validation, anti-cancer drug screening, and cell cycle/apoptosis studies. Representative assays include MTT, colony formation, flow cytometry for cell cycle analysis, western blotting, RT-qPCR, and xenograft tumor models. These polyclonal knockout cells provide a versatile platform for functional genomics and drug discovery. For additional information, please contact Ascent Research.
