The CCDC85C Knockout A2780 Polyclonal Cells product comprises a population of human A2780 ovarian carcinoma cells that have been subjected to CRISPR/Cas9-mediated gene disruption targeting the CCDC85C locus. This polyclonal cell pool, generated without single-cell cloning, provides a heterogeneous knockout model suitable for studying loss-of-function phenotypes in an ovarian cancer background. The polyclonal format preserves population-level diversity, reducing clonal artifacts while enabling robust detection of CCDC85C-dependent effects. The knockout is achieved through CRISPR/Cas9-induced double-strand breaks in the CCDC85C gene, leading to gene disruption across the cell pool.
The A2780 host cell line is a well-established human ovarian carcinoma epithelial cell line derived from an untreated patient. It is widely employed in ovarian cancer research, particularly for investigations into tumorigenesis, metastasis, and drug resistance mechanisms. A2780 cells harbor wild-type p53 and are sensitive to platinum-based chemotherapeutics, making them a valuable model for studying intrinsic and acquired resistance pathways. Their epithelial origin and adherent growth properties facilitate standard cell-based assays, including proliferation, migration, and colony formation studies.
CCDC85C encodes a coiled-coil domain-containing protein whose biological function remains largely uncharacterized. Coiled-coil domains are known to mediate protein-protein interactions, and CCDC85C is predicted to participate in homodimerization or heteromeric complexes. Although no definitive upstream regulators or downstream effectors have been identified, the structural features of CCDC85C suggest it may serve as a scaffold or adaptor protein in cellular signaling networks. Its potential role in regulating cytoskeletal organization or signal transduction pathways could influence cancer cell behavior, but direct evidence is lacking.
In the A2780 ovarian cancer context, knockout of CCDC85C provides a unique opportunity to interrogate its contribution to malignant phenotypes. Disruption of putative protein-protein interactions mediated by the coiled-coil domain may alter cell proliferation, migration, or survival pathways. Given the frequent dysregulation of scaffolding proteins in cancer, this knockout model can help reveal whether CCDC85C modulates key oncogenic processes. Comparative analysis between wild-type A2780 and the knockout polyclonal population allows for the assessment of CCDC85C-dependent changes in cellular functions, offering insights into its potential as a therapeutic target or biomarker.
This polyclonal knockout cell pool is ideally suited for a range of experimental applications, including functional genomics, protein interaction studies, and cancer biology research. Researchers can employ Western blotting and RT-qPCR to confirm knockout and assess downstream gene expression changes. Proliferation assays such as MTT and colony formation, along with migration and invasion assays, enable functional characterization of CCDC85C??s role in tumor cell behavior. Co-immunoprecipitation and RNA-seq experiments can further elucidate interaction partners and transcriptomic alterations. For detailed product inquiries and technical support, please contact Ascent Research.
