The DOCK2 Knockout NCI-H1703 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted disruption of the DOCK2 gene in the human non-small cell lung cancer (NSCLC) line NCI-H1703. This product provides a heterogeneous pool of cells carrying Cas9-mediated modifications at the DOCK2 locus, ensuring a robust loss-of-function model that avoids clonal artifacts. Researchers can use this system to interrogate DOCK2-mediated processes in lung squamous cell carcinoma without the biases introduced by single-cell clonal selection.
NCI-H1703 is a well-characterized human NSCLC cell line established from a squamous cell carcinoma of the lung. It is extensively employed for studies of EGFR signaling, drug sensitivity, and tumor cell migration. Expressing wild-type EGFR and retaining epithelial characteristics, these cells serve as an ideal platform for exploring the molecular mechanisms of carcinoma progression, particularly those involving small GTPase signaling and actin cytoskeletal dynamics.
DOCK2 encodes a guanine nucleotide exchange factor (GEF) that specifically activates the small GTPases Rac1 and Rac2. It functions downstream of chemokine receptors (CXCR4, CCR7), TCR/BCR stimulation, and cytokines (IL-2, IL-7). DOCK2 forms a complex with ELMO1 to catalyze GDP/GTP exchange on Rac, triggering PAK1 phosphorylation, WAVE complex recruitment, and Arp2/3-mediated actin polymerization to drive lamellipodia formation and cell migration. CrkL, Vav1, and PI3K integrate receptor and integrin signals, positioning DOCK2 as a critical node linking immune signals to the actin cytoskeleton. In immune cells, DOCK2 governs chemotaxis and synapse formation; its dysregulation may promote cancer cell invasion.
Disruption of DOCK2 in the NCI-H1703 lung carcinoma line provides a powerful model for dissecting Rac-mediated signaling in NSCLC. Elevated Rac activity is associated with enhanced migratory and invasive capacity, and DOCK2 may act as a context-specific GEF driving these phenotypes. This polyclonal knockout population enables analysis of actin dynamics, cell motility, and tumor-immune cell interactions in co-culture systems, offering insights into the tumor microenvironment.
This knockout product supports a broad range of functional assays. Wound healing and transwell migration/invasion assays quantify DOCK2-dependent motility, while Rac pull-down and phospho-PAK1 western blotting monitor pathway activity. Immunofluorescence visualizes actin reorganization and lamellipodia. Flow cytometry, RT-qPCR, and MTT assays allow receptor expression profiling, transcript analysis, and drug sensitivity testing. Co-IP for DOCK2-ELMO1 interactions and high-throughput inhibitor screening are also enabled. For further details, contact Ascent Research.
