The DOCK5 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human A2780 ovarian carcinoma cell line. This product provides a heterogeneous mixture of cells harboring CRISPR-mediated disruptions in the DOCK5 gene, enabling loss-of-function analyses without clonal bias. The polyclonal format is advantageous for initial functional screens and pathway studies where a representative knockout phenotype across a cell pool is sufficient.
The A2780 cell line originates from a human ovarian endometrioid adenocarcinoma and is a widely utilized model for ovarian cancer research. It is particularly valued for studies on drug resistance, notably to cisplatin and paclitaxel, and for investigating signal transduction pathways involved in tumor progression. The cells retain key oncogenic signaling networks, making them a relevant background for exploring gene function in ovarian carcinoma.
DOCK5 encodes a guanine nucleotide exchange factor (GEF) that activates the small GTPases Rac and Cdc42 by catalyzing GDP-to-GTP exchange. This GEF activity promotes actin cytoskeleton reorganization, cell migration, and adhesion. DOCK5 functions through an obligate interaction with ELMO1 and ELMO2, which mediate membrane recruitment and complex formation. Upstream signals from integrin receptors and receptor tyrosine kinases (EGFR, PDGFR) converge on DOCK5 via PI3K, while downstream effectors include PAK1, WAVE2, and the Arp2/3 complex, forming the DOCK5-ELMO-Rac1 axis central to cell motility.
In the A2780 ovarian cancer context, DOCK5 disruption allows direct investigation of its contribution to migratory, invasive, and adhesive properties critical for metastasis. Loss of DOCK5 function is expected to impair actin-dependent processes, potentially altering chemosensitivity and integrin-mediated signaling. The polyclonal population mirrors some degree of tumor heterogeneity, making it suitable for studying variable knockout effects on cancer cell behavior. This makes the cells a valuable tool for preclinical research into metastatic ovarian cancer.
Applications include wound healing and Transwell migration/invasion assays to measure motility, Rac/Cdc42 activation assays (G-LISA), western blotting for downstream effector phosphorylation, and immunocytochemistry for actin visualization. These cells enable mechanistic studies of chemokine- and integrin-dependent pathways in ovarian cancer. For additional information, contact Ascent Research.
