The CCDC102A Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the human CCDC102A gene. This product consists of a heterogeneous pool of HeLa cells carrying targeted disruptions of the CCDC102A locus, providing a versatile model to interrogate gene function without assumptions of clonal uniformity. The polyclonal format captures a range of editing outcomes, enabling robust assessment of phenotypic consequences while mitigating clonal artifacts. These cells serve as a foundational tool for investigators exploring the role of CCDC102A in cancer-relevant processes.
The host HeLa cell line is derived from a cervical adenocarcinoma and is one of the most widely used human cell lines in biomedical research. HeLa cells harbor integrated human papillomavirus type 18 (HPV18) DNA, leading to constitutive expression of the viral oncoproteins E6 and E7. These proteins inactivate tumor suppressors p53 and retinoblastoma protein (RB), respectively, driving uncontrolled proliferation and genomic instability. Consequently, HeLa cells represent a well-established model for studying HPV-driven carcinogenesis, cell cycle dysregulation, and therapeutic responses.
CCDC102A encodes a coiled-coil domain-containing protein predicted to facilitate protein-protein interactions, though its molecular function remains largely uncharacterized. Based on domain architecture, CCDC102A may participate in assembling macromolecular complexes involved in cytoskeletal organization or cell cycle progression. No upstream regulators, downstream targets, or interacting partners have been validated; however, its potential interaction networks are of significant interest. This knockout model enables systematic investigation of CCDC102A??s role through co-immunoprecipitation, proximity labeling, and functional rescue experiments to map its binding partners and downstream effectors.
In the context of HeLa cells, loss of CCDC102A offers a unique opportunity to explore its contribution to processes altered by HPV18 E6/E7 expression. Predicted functions in protein scaffolding and cytoskeletal dynamics suggest possible roles in cell morphology, adhesion, or migration??phenotypes frequently dysregulated in cervical cancer. Studies using this knockout pool may reveal whether CCDC102A intersects with oncogenic signaling or tumor suppressive pathways, providing insights into HPV18-associated malignancy and identifying potential vulnerabilities.
Typical research applications include functional characterization studies using western blotting to confirm knockout, immunofluorescence to assess protein localization, and cell-based assays such as proliferation, cell cycle analysis by flow cytometry, and migration assays to measure phenotypic changes. The polyclonal nature supports protein interaction network analysis via co-immunoprecipitation and facilitates drug target exploration by enabling high-throughput screening. This product is a valuable resource for investigators dissecting uncharacterized genes in cancer biology. For more information, please contact Ascent Research.
