The DOCK7 Knockout A2780 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of A2780 human ovarian adenocarcinoma cells with targeted disruption of the DOCK7 gene. This loss-of-function model is supplied as a heterogeneous polyclonal pool, ensuring broad representation of edited genotypes while effectively eliminating functional DOCK7 expression across the population. The cells are derived from the well-characterized A2780 host cell line and are maintained under standard adherent culture conditions, providing a robust system for interrogating DOCK7-dependent biology.
The A2780 cell line is a widely studied model of ovarian adenocarcinoma, originally established from an untreated patient. These epithelial cells exhibit adherent morphology and retain key characteristics of ovarian cancer, including rapid proliferation and metastatic potential. A2780 cells are routinely employed to investigate tumor progression, invasion, drug response, and signal transduction mechanisms, making them an ideal host for studying the role of DOCK7 in ovarian cancer pathology.
DOCK7 functions as a guanine nucleotide exchange factor (GEF) for the small GTPases Rac1 and Cdc42, forming a stable complex with ELMO1 or ELMO2 to facilitate GTP loading and activation. Active Rac1-GTP engages downstream effectors including PAK kinases and the WAVE regulatory complex, which in turn activates the Arp2/3 complex to drive branched actin polymerization and lamellipodia formation. This pathway is regulated by upstream inputs from integrin receptors, growth factor receptors, Rho GTPases, and PI3K, thereby linking extracellular adhesion and growth signals to cytoskeletal reorganization. In DOCK7-knockout cells, Rac1 activation is impaired, disrupting the signaling cascade from PAK1 to WAVE2 and Arp2/3, ultimately attenuating actin-based cell motility and invasive behavior.
In the context of A2780 ovarian cancer cells, DOCK7 plays a pivotal role in promoting Rac1-driven migration and invasion, processes essential for metastasis. Loss of DOCK7 compromises the formation of Rac1-GTP and suppresses cytoskeletal dynamics, leading to reduced lamellipodial protrusion and diminished invasive capacity. Consequently, this knockout model provides a powerful experimental system for dissecting the molecular mechanisms underlying ovarian cancer metastasis and for evaluating therapeutic strategies that target GTPase-mediated cell motility and the DOCK7-ELMO signaling axis.
Researchers can employ these polyclonal knockout cells in a variety of functional assays, including Rac1-GTP pull-down experiments coupled with western blotting to quantify active Rac1 levels, transwell migration and invasion assays to assess metastatic potential, and phalloidin staining to visualize F-actin reorganization. Immunofluorescence detection of total and phosphorylated PAK offers a direct readout of downstream pathway activation. Additionally, RNA-seq transcriptomic analysis can reveal global expression changes upon DOCK7 loss, while cell proliferation assays evaluate growth phenotypes. These cells are also suitable for screening chemical probes that modulate the DOCK7-ELMO interaction and for testing how DOCK7-dependent signaling affects drug sensitivity. For further details, please contact Ascent Research.
