The DOCK11 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma cell line, engineered for targeted disruption of the DOCK11 gene. This loss-of-function model enables investigation of DOCK11-dependent processes without the confounding effects of residual protein expression. The polyclonal format provides a heterogeneous knockout population suitable for functional genomic studies, phenotypic screening, and pathway analysis in a gastric cancer context.
The HGC-27 cell line is an epithelial gastric cancer model originally established from the lymph node metastasis of a gastric adenocarcinoma in a 35-year-old male patient. HGC-27 cells exhibit key characteristics of gastric carcinoma, including invasive potential and dysregulated signaling networks, making them a relevant system for studying tumor progression and metastasis. Their epithelial origin and metastatic derivation provide a clinically pertinent backdrop for exploring the molecular underpinnings of gastric cancer cell motility and invasion.
DOCK11 (dedicator of cytokinesis 11) functions as a guanine nucleotide exchange factor (GEF) that specifically activates the small GTPases CDC42 and RAC1 by catalyzing GDP-to-GTP exchange. This activation triggers downstream effectors such as PAK kinases, the WAVE complex, and the ARP2/3 complex, promoting actin polymerization, filopodia formation, and cytoskeletal reorganization. DOCK11 operates in a signaling complex with ELMO1 and responds to upstream signals from receptor tyrosine kinases (e.g., EGFR), chemokine receptors, and PI3K, thereby integrating extracellular cues with cytoskeletal dynamics. Through these interactions, DOCK11 critically regulates cell migration, immune cell signaling, and cancer cell invasion.
In the HGC-27 gastric carcinoma model, loss of DOCK11 disrupts the CDC42/RAC1 signaling axis, providing a powerful tool to dissect the role of actin cytoskeleton remodeling in gastric cancer invasion and metastasis. The polyclonal knockout population allows researchers to evaluate the overall impact of DOCK11 ablation on cell motility, chemotaxis, and interactions with the tumor microenvironment. Additionally, given the involvement of DOCK11 in immune cell function, this model may be leveraged to study immunomodulatory aspects of gastric cancer and validate DOCK11 as a potential therapeutic target.
Researchers can employ this knockout cell population in a variety of assays, including western blotting and RT-qPCR for knockout verification and downstream target expression analysis, GTPase activation pull-down assays to assess CDC42/RAC1 activity, Transwell migration and invasion assays to measure metastatic potential, and immunofluorescence to visualize F-actin reorganization. Co-immunoprecipitation experiments can confirm the disruption of DOCK11-ELMO1 complexes, while phospho-PAK analysis and flow cytometry for immune activation markers extend utility into signal transduction and immunology studies. For further information, please contact Ascent Research.
