The DLGAP5 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma epithelial cell line HGC-27. This product comprises a heterogeneous pool of cells carrying targeted disruptions in the DLGAP5 gene locus, generated through CRISPR/Cas9-mediated gene editing without clonal selection, enabling the study of DLGAP5 loss-of-function within a diverse genetic background. The polyclonal format preserves biological variability and avoids artifacts associated with single-cell cloning, making it suitable for experiments where population-level phenotypes are interrogated. As a polyclonal knockout model, it is not characterized by a uniform mutation type or zygosity, and users should anticipate a range of editing outcomes across the cell population.
The host HGC-27 cell line is an adherent, tumorigenic gastric carcinoma epithelial line originally established from the metastatic lymph node of a patient with gastric cancer. HGC-27 cells exhibit characteristics of poorly differentiated adenocarcinoma and are widely employed as a model system for studying gastric cancer biology, including tumor growth, invasion, and metastatic potential. Their derivation from a metastatic site makes them particularly relevant for investigating molecular mechanisms that drive gastric cancer progression and dissemination. This cell line retains key oncogenic signaling pathways and provides a clinically relevant context for evaluating gene function in gastric malignancies.
DLGAP5 (discs large-associated protein 5), also known as HURP, encodes a microtubule-associated protein essential for mitotic spindle assembly and stabilization. The protein functions by bundling microtubules and recruiting Aurora B kinase to kinetochores through direct interactions with the chromosomal passenger complex components INCENP, Survivin, and Borealin. This interaction ensures proper Aurora B localization and activity, which is critical for correcting erroneous kinetochore?Cmicrotubule attachments and facilitating chromosome alignment. DLGAP5 expression is transcriptionally regulated by FOXM1 and E2F1, and its activation is coupled to cell cycle progression via phosphorylation by the CDK1/cyclin B complex. Downstream, DLGAP5-mediated microtubule bundling and Aurora B targeting promote faithful chromosome segregation and genomic stability.
Upregulation of DLGAP5 is observed in multiple cancers, including gastric, hepatocellular, and breast carcinomas, where it is associated with chromosomal instability and poor clinical prognosis. In HGC-27 gastric cancer cells, DLGAP5 overexpression may contribute to aberrant mitotic progression and aneuploidy, fueling tumor heterogeneity and aggressiveness. Disruption of DLGAP5 using this polyclonal knockout model allows researchers to dissect its role in gastric cancer mitosis, evaluate consequences on spindle morphology and chromosome segregation fidelity, and assess its impact on tumorigenic properties such as proliferation, migration, and drug sensitivity.
This polyclonal DLGAP5 knockout cell pool is optimized for a range of functional assays, including western blotting to confirm DLGAP5 loss, immunofluorescence analysis of spindle architecture and chromosome alignment, and flow cytometry-based cell cycle profiling. It is well-suited for proliferation (MTT), apoptosis, and migration/invasion studies to delineate DLGAP5 contributions to gastric cancer aggressiveness. Transcriptomic analysis by RNA-seq can reveal downstream gene expression changes, while drug sensitivity screening, particularly against Aurora kinase inhibitors, can identify therapeutic vulnerabilities. For further details, please contact Ascent Research.
