The CCDC167 Knockout HGC-27 Polyclonal Cells product provides a heterogeneous population of CRISPR/Cas9-edited HGC-27 cells with targeted disruption of the CCDC167 gene. This ready-to-use polyclonal knockout pool enables loss-of-function analysis without requiring single-cell cloning or selection of a specific clonal isolate. The polyclonal format retains biological variability while ensuring robust gene ablation across the population, making it suitable for pooled screening applications and functional assays where cellular heterogeneity is acceptable.
HGC-27 is a human gastric carcinoma cell line originally derived from the metastatic lymph node of a patient with gastric adenocarcinoma. It is widely employed as a model for gastric cancer biology, particularly in studies of tumor invasion, metastasis, and drug sensitivity. The cell line exhibits features of epithelial-derived tumor cells and is commonly used to investigate molecular mechanisms driving gastric cancer progression and therapeutic resistance. Its genetic background includes chromosomal abnormalities typical of gastric cancers, providing a relevant context for studying genes involved in maintaining genomic stability.
CCDC167 (Coiled-Coil Domain Containing 167) encodes a centrosome- and spindle pole-associated protein that contains a coiled-coil domain, facilitating protein-protein interactions critical for mitotic spindle organization. CCDC167 is temporally regulated by the master mitotic kinases CDK1 and PLK1, which phosphorylate or direct its localization during cell cycle progression. At the mitotic spindle, CCDC167 interacts with the kinetochore-associated proteins CENPF and NDC80, as well as with spindle assembly checkpoint components. Downstream, CCDC167 contributes to the recruitment and stabilization of microtubule-associated proteins and the chromosomal passenger complex, thereby ensuring proper chromosome alignment and segregation. In concert with CCNB1-CDK1, PLK1, and Aurora kinases, CCDC167 is positioned within a network that governs mitotic fidelity.
In the context of HGC-27 gastric adenocarcinoma cells, knockout of CCDC167 is predicted to compromise mitotic spindle integrity, leading to mitotic errors such as chromosome missegregation and aneuploidy. This model therefore provides a physiologically relevant system to investigate the contribution of mitotic defects to the chromosomal instability characteristic of advanced gastric cancers. By disrupting CCDC167 function, researchers can examine how impaired mitotic regulation affects tumor cell proliferation, genomic instability, and response to spindle-targeting chemotherapeutic agents, potentially revealing vulnerabilities unique to gastric cancer cells with high mitotic dependency.
This polyclonal knockout cell pool is intended for a variety of investigative applications. Researchers can employ western blotting to assess changes in cell cycle regulators (e.g., cyclin B1, phospho-histone H3) and apoptosis markers. Immunofluorescence microscopy with antibodies against ??-tubulin and pericentrin allows detailed visualization of spindle and centrosome morphology. Flow-cytometric cell cycle analysis quantifies alterations in DNA content profiles, while proliferation and apoptosis assays evaluate the functional consequences of CCDC167 loss. Transcriptomic analysis via RNA-seq can further elucidate gene expression changes underlying observed phenotypes. For technical specifications and ordering information, please contact Ascent Research.
