The DOCK4 Knockout A2780 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human A2780 ovarian cancer epithelial cell line. This product carries a targeted disruption of the DOCK4 gene, resulting in loss of DOCK4 protein function across a heterogeneous pool of edited cells. The polyclonal format provides a robust and physiologically relevant model for investigating DOCK4-dependent processes without the clonal bias inherent in monoclonal derivatives. Researchers can employ this knockout population to dissect the contributions of DOCK4 to cell signaling, migration, and invasion within the context of ovarian adenocarcinoma.
The parental A2780 cell line was established from an untreated ovarian endometrioid adenocarcinoma patient and is widely utilized as a model for ovarian cancer biology. These adherent epithelial cells retain key characteristics of the original tumor, including genetic alterations associated with ovarian carcinogenesis, making them particularly suitable for studying pathways implicated in tumor progression and metastatic dissemination. The A2780 background offers a well-characterized platform for functional genomics experiments and drug response assays, with extensive published data available for comparative analyses.
DOCK4 functions as a guanine nucleotide exchange factor (GEF) dedicated to the activation of Rac1 GTPase, catalyzing the exchange of GDP for GTP to promote Rac1-dependent signaling. Rac1 activation triggers downstream effectors such as PAK kinases and the WAVE regulatory complex, which nucleate actin polymerization through the Arp2/3 complex, leading to cytoskeletal rearrangements that govern cell migration, adhesion, and invasion. DOCK4 activity is regulated upstream by integrin ??v??3, ELMO2, and phosphatidylinositol 3-kinase, and it engages in direct protein?Cprotein interactions with ELMO2 and CrkII via SH3 domain modules. This signaling network couples extracellular cues to dynamic reorganization of the actin cytoskeleton and focal adhesion turnover.
In ovarian cancer, DOCK4-mediated Rac1 activation has been implicated in driving metastatic progression and tumor invasion. The A2780 ovarian adenocarcinoma model, with its known propensity to mimic peritoneal dissemination when placed in appropriate in vivo settings, offers a pertinent cellular context for interrogating the role of DOCK4 in aggressive ovarian cancer phenotypes. Disrupting DOCK4 in this background enables researchers to assess how Rac1-dependent pathways contribute to the invasive capacity of ovarian cancer cells and to evaluate the functional consequences on actin dynamics, cell-matrix interactions, and potentially on resistance to therapeutic interventions targeting metastatic spread.
Typical applications of the DOCK4 Knockout A2780 Polyclonal Cells include western blotting to confirm loss of DOCK4 expression and to measure Rac1-GTP levels, Transwell migration and invasion assays to quantify metastatic potential, immunofluorescence staining of F-actin to visualize cytoskeletal alterations, and phospho-PAK detection to monitor downstream signaling activity. These cells are also well suited for transcriptomic profiling via RNA-seq and for drug screening campaigns focused on metastasis inhibitors. For technical inquiries or assistance with experimental design, please contact Ascent Research.
