The DLGAP5 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population, providing a loss-of-function model for the gene encoding discs large-associated protein 5 (DLGAP5). Generated via CRISPR/Cas9-mediated gene disruption in the AGS human gastric adenocarcinoma cell line, this population comprises a heterogeneous pool of cells with targeted disruption of the DLGAP5 locus, enabling functional studies without single-cell clonal selection. This reagent is intended for use in advanced biomedical research applications requiring precise gene ablation in epithelial-derived gastric cancer models.
The AGS host cell line is a well-established adherent epithelial cell model originally derived from a human gastric adenocarcinoma. These cells exhibit characteristic epithelial morphology and serve as a representative system for studying gastric adenocarcinoma biology, including proliferation, signaling, and therapeutic response. The AGS line is widely utilized in cancer research due to its robust growth properties and relevance to gastric tumorigenesis, making it an appropriate host for interrogating the role of mitotic regulators like DLGAP5 in stomach cancer.
DLGAP5 is a microtubule-associated protein critical for mitotic spindle assembly and chromosome congression. It functions by binding and stabilizing microtubules, a process regulated through phosphorylation by Aurora kinase A. DLGAP5 acts downstream of Aurora A and the TPX2 complex, interacting directly with Aurora A, microtubules, and Kinesin-5 to ensure proper spindle bipolarity and kinetochore?Cmicrotubule attachments. Transcriptional regulation of DLGAP5 is mediated by E2F transcription factors, linking its expression to cell cycle progression. Disruption of DLGAP5 compromises spindle integrity, leading to chromosome misalignment, aberrant mitotic progression, and potential triggering of mitotic catastrophe or apoptosis.
In the context of AGS human gastric adenocarcinoma cells, DLGAP5 knockout provides a powerful platform for dissecting mitotic signaling pathways that drive tumor cell proliferation and genomic instability. Overexpression of DLGAP5 is associated with poor prognosis in gastric adenocarcinoma, hepatocellular carcinoma, colorectal cancer, and breast cancer, highlighting its oncogenic potential. By eliminating DLGAP5 function, researchers can investigate its contribution to gastric cancer cell growth, evaluate dependency on Aurora A signaling, and explore downstream effects on microtubule dynamics and cell cycle checkpoints specifically within an epithelial gastric cancer background.
Typical research applications for this knockout model include high-throughput screening for mitotic inhibitors, functional genomics studies, drug target validation, and detailed cell cycle analyses using representative assays such as immunofluorescence for mitotic spindle morphology, flow cytometry for cell cycle distribution, western blotting for DLGAP5 and phospho-Aurora A, proliferation assays, RNA-seq transcriptomics, and apoptosis detection. These polyclonal cells are suitable for short-term functional experiments, comparison with wild-type AGS cells, and as a tool for preclinical gastric cancer research. For detailed protocol support and further information, please contact Ascent Research.
