The DOCK7 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population originating from the human gastric adenocarcinoma cell line AGS. This product comprises a mixed population of cells with targeted disruptions in the DOCK7 gene, enabling loss-of-function studies without clonal selection. The polyclonal format provides a heterogeneous model system for investigating DOCK7-dependent processes in an epithelial gastric cancer context.
The AGS cell line was derived from a human gastric adenocarcinoma and exhibits adherent epithelial morphology. Widely used in gastric cancer research, AGS cells serve as a robust in vitro model for studying tumor cell signaling, proliferation, and therapeutic drug responses. Their well-characterized background supports the generation of gene knockouts to dissect oncogenic mechanisms relevant to gastric adenocarcinoma.
DOCK7 functions as a guanine nucleotide exchange factor (GEF) that activates Rac1 and Cdc42 GTPases by promoting GDP-to-GTP exchange. This activation orchestrates actin cytoskeletal remodeling and cell migration. DOCK7 is regulated by upstream inputs from PI3K/PIP3, integrin adhesion, and receptor tyrosine kinases including EGFR and FGFR. It cooperates with ELMO scaffolding proteins to efficiently catalyze nucleotide exchange on Rac1/Cdc42, leading to downstream signaling via PAK kinase, the Arp2/3 complex, and MAP kinase pathways such as JNK and p38. Additionally, DOCK7 interacts with TACC3 to influence microtubule dynamics, integrating actin and microtubule networks.
In the context of AGS gastric cancer cells, knockout of DOCK7 is expected to disrupt Rac1/Cdc42-mediated actin reorganization, thereby impairing migratory and invasive capacities. This model enables investigation of signaling crosstalk between Rac/Cdc42 pathways and mTOR/ERK cascades, which are frequently dysregulated in gastric cancer. The polyclonal knockout population reflects heterogeneous genetic backgrounds, making it suitable for studying the dominant effects of DOCK7 loss on tumor cell behavior.
The knockout cells are optimized for cell migration and invasion assays (Transwell), immunofluorescence visualization of the actin cytoskeleton, and biochemical readouts such as Rac1/Cdc42 activation (G-LISA) and phospho-signaling analysis of PAK and JNK. They also support expression analysis via western blotting and RT-qPCR, co-immunoprecipitation of DOCK7?CELMO complexes, and screening for pathway inhibitors. The model can be applied to neurological disease research related to DOCK7 mutations in epileptic encephalopathy and microcephaly. For further information, contact Ascent Research.
