The CCDC82 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the CCDC82 gene in AGS cells. This product provides a versatile loss-of-function model for investigating CCDC82, a microtubule-associated coiled-coil protein implicated in mitotic spindle orientation and cell division. The polyclonal nature yields a heterogeneous pool of cells harboring diverse gene disruptions, enabling population-level functional studies without clonal isolation. This knockout model is suitable for dissecting CCDC82-dependent mechanisms in mitosis and cancer biology.
The host AGS cell line is derived from a human gastric adenocarcinoma of a 54-year-old female and exhibits adherent epithelial morphology. AGS cells are widely employed as a gastric epithelial model for cancer research, including studies of Helicobacter pylori pathogenesis, epithelial barrier integrity, and tumor cell signaling. The gastric adenocarcinoma background offers a physiologically relevant system to examine how CCDC82 loss influences mitotic fidelity and malignant progression.
CCDC82 encodes a coiled-coil domain protein that localizes to spindle microtubules and is essential for proper mitotic spindle orientation. It acts by recruiting the cortical LGN (GPSM2)/NuMA (NUMA1) complex, which in turn anchors the dynein-dynactin motor complex to generate pulling forces on astral microtubules. Upstream mitotic kinases, including Aurora A, CDK1, and PLK1, as well as RanGTP, regulate CCDC82 localization and function. Through these interactions, CCDC82 ensures accurate chromosome segregation and prevents genomic instability. Disruption of CCDC82 is predicted to impair spindle positioning, leading to mitotic errors.
In the AGS gastric adenocarcinoma model, knockout of CCDC82 may produce aberrant mitotic spindle orientation, contributing to asymmetric cell division, chromosomal missegregation, and genomic instability??features intimately linked to cancer progression. This model facilitates exploration of how spindle orientation defects promote aneuploidy and tumorigenic phenotypes in gastric epithelial cells. Moreover, it enables investigation of potential synthetic lethal vulnerabilities or therapeutic weaknesses that arise specifically upon CCDC82 loss in a gastric cancer context.
Researchers can utilize this polyclonal knockout population in a variety of functional assays, including Western blotting to assess CCDC82 protein depletion, immunofluorescence microscopy to examine spindle orientation defects, flow cytometry for cell cycle profiling, and live-cell imaging to monitor mitotic progression and errors. Additional applications encompass colony formation assays to evaluate proliferative capacity and wound healing migration assays to study cell motility changes. This model is particularly valuable for dissecting the molecular circuitry of mitotic spindle orientation, testing CCDC82 as a candidate therapeutic target in gastric cancer, and screening for modulators of mitotic fidelity. For further inquiries or to obtain a quote, please contact Ascent Research.
