This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line, designed to disrupt the DOCK5 gene. The polyclonal format provides a heterogeneous mixture of cells bearing diverse gene-editing events, enabling robust loss-of-function studies without clonal selection artifacts. This knockout model serves as a powerful tool for dissecting DOCK5-dependent signaling mechanisms in a metastatic gastric cancer context.
HGC-27 cells were originally isolated from a lymph node metastasis of a gastric adenocarcinoma in a Japanese male. As a widely used metastatic gastric cancer cell line, HGC-27 retains key features of epithelial tumor cells with high invasive and migratory capacity. Its derivation from a secondary tumor site makes it particularly suitable for studying molecular pathways that drive gastric cancer dissemination and metastasis.
DOCK5 encodes a guanine nucleotide exchange factor (GEF) that specifically activates the small GTPase Rac1 by catalyzing GDP-to-GTP exchange. This activation is triggered by upstream integrin signaling and receptor tyrosine kinases such as EGFR, in concert with adaptor proteins CrkII and the ELMO1/ELMO2 complex. Active Rac1 then engages downstream effectors including PAK1, which in turn stimulates the WAVE regulatory complex and the Arp2/3 complex to promote branched actin polymerization and lamellipodia formation. DOCK5 thus forms a critical hub linking extracellular adhesion and growth factor cues to cytoskeletal remodeling, focal adhesion dynamics, and directional cell migration.
In DOCK5 knockout HGC-27 polyclonal cells, Rac1 activation is significantly impaired, leading to compromised actin-driven membrane protrusion and reduced cell motility. This defect directly attenuates the invasive phenotype characteristic of the parental line, offering a physiologically relevant model for studying the molecular basis of gastric cancer metastasis. The knockout cells enable researchers to assess the dependence of metastatic traits on DOCK5-mediated Rac1 signaling and to evaluate compensatory pathways that may emerge upon disruption of this axis.
Typical research applications include mechanistic investigations of DOCK5-driven cell migration and invasion using Boyden chamber assays, time-lapse imaging, and quantitative actin cytoskeleton staining. The model supports pharmacologic screening for Rac1 pathway inhibitors by combining endpoint assays such as G-LISA Rac1 activity measurements with Western blotting and RT-qPCR analysis of downstream targets. Researchers can also integrate focal adhesion analysis and immunofluorescence to map DOCK5-interacting partners like ELMO1 and FAK. For further technical information or customized cell products, please contact Ascent Research.
