The CCDC85C Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A-549 lung adenocarcinoma cell line. This product provides a heterogeneous pool of cells with targeted disruption of the CCDC85C gene, enabling loss-of-function studies. The polyclonal nature ensures diverse editing outcomes across the population, representing a robust model for functional genomics. These cells are designed for researchers investigating the role of CCDC85C in cancer biology, with a focus on its interactions with DISC1 and its impact on microtubule dynamics and cell cycle regulation.
The parental A-549 cell line originates from a 58-year-old Caucasian male with lung adenocarcinoma, making it a widely employed model for non-small cell lung cancer (NSCLC) research. As an epithelial cell line, A-549 retains key characteristics of alveolar type II pneumocytes, offering a physiologically relevant context for studying lung cancer pathogenesis. This cell line is extensively used in cancer biology, drug screening, and signal transduction studies due to its well-defined genetic background and reproducible growth properties. Its adherent monolayer growth facilitates imaging and biochemical assays, enhancing experimental versatility.
CCDC85C encodes a coiled-coil domain-containing protein that interacts with DISC1, a scaffold protein implicated in centrosomal function and microtubule organization. Through this interaction, CCDC85C is thought to modulate microtubule dynamics and cell cycle progression, likely via the DISC1?CGSK3?¨C??-catenin signaling axis. GSK3?? and ??-catenin are known downstream effectors of DISC1, and their activity influences cell proliferation and migration. Although upstream regulators of CCDC85C remain unknown, its association with DISC1 positions it within a regulatory network critical for maintaining centrosome integrity and mitotic fidelity. Disruption of CCDC85C may therefore perturb these processes, providing a mechanistic basis for its study in cancer.
In A-549 cells, which harbor mutations in key tumor suppressors and oncogenes, the knockout of CCDC85C offers a powerful tool to dissect its contribution to lung adenocarcinoma pathogenesis. Given the role of DISC1 signaling in cell cycle control and microtubule organization, loss of CCDC85C may lead to altered proliferation rates, defective mitotic spindle formation, or enhanced sensitivity to chemotherapeutic agents. This model is particularly suited for exploring how centrosomal proteins influence NSCLC progression and for evaluating the therapeutic potential of targeting the DISC1 interactome. The polyclonal population reflects the heterogeneity often observed in tumor samples, enhancing translational relevance.
Typical research applications include functional investigation of CCDC85C in lung adenocarcinoma, delineation of DISC1-mediated signaling pathways, and assessment of cell proliferation and migration. The polyclonal knockout cells are compatible with a range of assays, including Western blotting, RT-qPCR, immunofluorescence, co-immunoprecipitation, and proliferation and migration assays. They serve as a valuable resource for drug response profiling and for identifying synthetic lethal interactions in NSCLC. For technical specifications or ordering details, please contact Ascent Research.
