The DOCK2 Knockout AGS Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DOCK2 gene in AGS human gastric adenocarcinoma cells. The polyclonal format minimizes clonal artifacts and supports population-level analyses, making it ideal for pooled functional screens, bulk migration studies, and biochemical assays. By disrupting DOCK2, this model enables investigation of Rac1-driven signaling pathways central to cytoskeletal reorganization and cellular motility in a gastric cancer context.
AGS cells are a widely used model for human gastric adenocarcinoma, retaining key features such as anchorage-independent growth and invasive capacity. This host line enables dissection of oncogenic signaling networks, particularly those involving Rho GTPases and chemokine receptors, that drive gastric cancer progression. Paired with targeted DOCK2 disruption, AGS cells allow precise interrogation of actin remodeling and invasion pathways in a disease-relevant background.
DOCK2 is a Rac1-specific guanine nucleotide exchange factor (GEF) that catalyzes GDP-GTP exchange, leading to actin polymerization, lamellipodia formation, and cell migration. Upstream regulators CXCR4, TCR, CD28, and PI3K modulate DOCK2 activity, while interaction with ELMO1, ELMO2, and CrkL facilitates Rac1 activation. Downstream, Rac1-GTP activates PAK kinases, JNK, and p38 MAPK, culminating in cytoskeletal reorganization via LIMK-cofilin and Arp2/3-mediated actin branching. This module is critical for immune cell motility and is co-opted by cancer cells to drive invasion and metastasis.
In gastric cancer, DOCK2-mediated Rac activation enhances malignant phenotypes by driving actin-based motility and matrix invasion. Aberrant DOCK2 expression correlates with increased metastatic potential and poor prognosis. Disruption of DOCK2 in AGS cells allows direct assessment of Rac1’s contribution to invasive behavior, identification of downstream transcriptional changes, and exploration of crosstalk with integrin adhesion pathways, providing a valuable system for uncovering metastatic mechanisms and testing therapeutic interventions.
The DOCK2 Knockout AGS Polyclonal Cells support diverse research applications. Western blotting verifies DOCK2 ablation and Rac1-GTP levels; Transwell and wound-healing assays quantify migration/invasion; immunofluorescence visualizes F-actin. Phospho-PAK ELISA monitors downstream signaling, and RNA-seq profiles DOCK2-dependent transcription. These cells are suitable for high-content screening of anti-motility compounds and co-culture models of tumor?Cimmune interactions. For further details or a quotation, contact Ascent Research.
