The EHD2 Knockout HGC-27 Polyclonal Cells are a heterogeneous pool of CRISPR/Cas9-edited gastric adenocarcinoma cells with targeted disruption of the EHD2 gene. This polyclonal knockout cell population provides a physiologically relevant loss-of-function model to investigate EHD2-dependent mechanisms within a gastric cancer background. By ablating EHD2 expression across a mixed population, the model facilitates robust assessment of gene function while mitigating clonal bias that may arise in monoclonal isolates.
HGC-27 cells constitute an extensively characterized epithelial cell line derived from the metastatic lymph node of a gastric adenocarcinoma patient. As a widely adopted model in gastric cancer research, these cells retain key molecular features of adenocarcinoma pathology, including dysregulated growth signaling, invasive potential, and altered adhesion properties. Their metastatic origin renders them particularly suited for studies exploring tumor dissemination, epithelial-to-mesenchymal transition, and interaction with the tumor microenvironment.
EHD2 encodes a dynamin-related ATPase that governs endocytic recycling of integrin receptors, orchestrating cell adhesion, spreading, and migration. It acts downstream of TGF-?? and Wnt signaling cascades, with mechanical stretch and transcriptional regulators such as p53 and serum response factor (SRF) further modulating its expression. EHD2 physically interacts with Syndapin II, SNAP29, Caveolin-1, and EHD1, and couples to actin polymerization and Rho GTPases like Rac1 and Cdc42. Through its control of Integrin ??1 and Rab11/Arf6-dependent trafficking routes, EHD2 critically influences focal adhesion kinase (FAK)/Src signaling and Smad2/Smad3-mediated transcriptional programs.
Disruption of EHD2 in the HGC-27 background destabilizes integrin-dependent adhesion platforms, likely impairing directed cell migration and invasion. Given the central role of EHD2 in linking endocytic trafficking to cytoskeletal dynamics, its loss can perturb the balance between pro-adhesive and pro-migratory signaling, potentially attenuating metastatic behavior. Moreover, because TGF-?? and Wnt pathways are frequently hyperactivated in gastric adenocarcinoma, EHD2 knockout cells offer a valuable tool to dissect crosstalk between these oncogenic signals and adhesion turnover in a disease-relevant setting.
Principal applications include mechanistic studies of EHD2 in gastric cancer cell migration and invasion, high-content imaging of integrin trafficking using immunofluorescence microscopy, and quantitative assessment of cell surface integrin levels via flow cytometry. The model is also suitable for drug screening campaigns targeting metastasis inhibition, co-immunoprecipitation to map EHD2 interactomes, phospho-signaling analyses of FAK and Smad effectors, and transcriptomic profiling by RNA-seq. For further technical specifications or ordering information, please contact Ascent Research.
