CCDC7 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the CCDC7 gene. This product consists of a heterogeneous mixture of HeLa cells that have undergone CRISPR/Cas9-mediated disruption of CCDC7, enabling researchers to examine the cellular consequences of CCDC7 ablation without clonal selection bias. The polyclonal format preserves genetic diversity and is well-suited for pooled functional assays, where the average effect of gene knockout is assessed across a bulk population.
The HeLa host cell line is an immortalized human cervical adenocarcinoma epithelial line originally derived from an HPV18-positive tumor. HeLa cells are widely used in biomedical research due to their robust growth and well-characterized molecular features. HPV18-mediated inactivation of p53 and Rb creates a unique genetic context that facilitates studies on how additional gene disruptions, such as CCDC7 knockout, alter cancer cell behavior. This cell line is commonly employed in signal transduction, drug discovery, and DNA repair investigations.
CCDC7 encodes a coiled-coil domain protein that functions in the DNA damage response. Upon DNA damage, ATM and ATR kinases phosphorylate CCDC7, promoting its interaction with 14-3-3 proteins and CHK1. This complex inactivates CDC25C to induce cell cycle arrest and modulates BCL-2 family members, upregulating BAX and downregulating BCL-2, to trigger apoptosis. CCDC7 also interacts with ATRIP and acts downstream of CHK2, integrating ATM and ATR signaling networks. These interactions position CCDC7 at a critical nexus of DNA repair, checkpoint control, and apoptosis.
In HeLa cells, CCDC7 knockout compromises the DNA damage response, potentially increasing genomic instability and sensitivity to genotoxic agents. This model is relevant for cervical cancer research, as CCDC7 has been linked to cancer predisposition and tumor suppression. By disrupting CCDC7 in HPV18-positive cells, researchers can explore how viral oncoproteins intersect with DNA repair pathways, uncovering synthetic lethal interactions or therapeutic targets for cervical cancer treatment.
The CCDC7 Knockout HeLa Polyclonal Cells are ideally suited for a wide range of experimental applications. Western blotting can validate loss of CCDC7, while immunofluorescence for ??H2AX foci measures DNA breaks. Flow cytometry assays cell cycle distribution, and Annexin V staining quantifies apoptosis. Colony formation assays measure clonogenic survival after genotoxic stress, and Comet assays directly visualize DNA strand breaks. RT-qPCR monitors expression of BAX and BCL-2. These tools support mechanistic studies of DNA damage signaling, screening for DNA repair inhibitors, and assessment of chemosensitivity in a cancer-relevant model. For further details, please contact Ascent Research.
