The DLGAP5 Knockout A2780 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human ovarian carcinoma cell line A2780. This loss-of-function model features targeted disruption of the DLGAP5 gene, generated through CRISPR/Cas9-mediated gene editing. The resulting polyclonal population comprises a heterogeneous mixture of edited alleles, offering a robust system for studying DLGAP5-dependent functions without the selection bias of clonal isolation.
The A2780 parental line is a well-characterized epithelial cell model established from an ovarian carcinoma of a chemotherapy-na?ve patient. Widely used in ovarian cancer research, A2780 cells exhibit responsiveness to platinum-based drugs and taxanes, making them particularly suitable for investigating mechanisms of drug sensitivity and resistance. This cell line retains key features of high-grade serous ovarian carcinoma and provides a physiologically relevant context for examining mitotic spindle regulators and their roles in tumor cell proliferation.
DLGAP5 (discs large-associated protein 5) functions as a critical spindle assembly factor during mitosis. It is activated downstream of Aurora A kinase and is transcriptionally regulated by E2F transcription factors and FOXM1. DLGAP5 interacts with Aurora A, TPX2, importin-??, and microtubules to stabilize spindle microtubules and recruit kinetochore proteins such as NDC80, thereby promoting correct chromosome alignment and kinetochore-microtubule attachment. Through these interactions, DLGAP5 ensures faithful chromosome segregation and progression through the G2/M transition; its depletion triggers mitotic arrest and subsequent apoptosis.
In A2780 cells, which are frequently employed to study chromosomal instability and mitotic vulnerabilities in ovarian cancer, DLGAP5 knockout offers a powerful tool to dissect the Aurora A?CTPX2?CDLGAP5 axis. Given that DLGAP5 is often overexpressed in ovarian, hepatocellular, lung, and breast cancers and correlates with poor prognosis, this model enables investigation of how its loss impacts mitotic fidelity, cell cycle progression, and survival in a disease-relevant background. Additionally, the polyclonal nature mitigates clonal artifacts and preserves population-level heterogeneity, closely mimicking the genetic variability encountered in tumor samples.
Researchers can employ this knockout cell population to investigate mitotic regulation, screen for synthetic lethal interactions, and evaluate sensitivity to anti-mitotic agents such as paclitaxel. Typical assays include western blotting to confirm DLGAP5 protein loss, immunofluorescence to visualize mitotic spindle defects, flow cytometry for cell cycle analysis, and apoptosis or proliferation assays. The model is also suited for functional genomics screens aimed at identifying genes whose depletion synergizes with DLGAP5 loss. For further information or technical inquiries, please contact Ascent Research.
