EHD2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated to disrupt the EHD2 gene in the AGS human gastric adenocarcinoma cell line. This loss-of-function model provides a heterogeneous pool of edited cells, enabling robust assessment of EHD2-dependent phenotypes in a gastric epithelial context without clonal selection artifacts.
The AGS cell line, originally derived from a 54-year-old female patient, is a well-established model for human gastric adenocarcinoma. These adherent epithelial cells display characteristic gastric epithelial markers and are widely employed to study gastric cancer cell biology, including signaling, proliferation, migration, and drug response. Their tumorigenic properties and genetic background resembling gastric cancer make them an ideal host for investigating genes involved in gastric cancer progression.
EHD2 encodes an ATPase that functions in endocytic recycling and caveolae dynamics. At the molecular level, EHD2 interacts with caveolin-1, actin, the Arp2/3 complex, and paxillin to stabilize caveolar invaginations and mediate their internalization. It is regulated upstream by signaling inputs from the epidermal growth factor receptor (EGFR), integrin-mediated adhesion, and Src family kinases. Downstream, EHD2 controls Rac1 activity and actin polymerization through the Arp2/3 complex, thereby modulating MAPK signaling and cytoskeletal reorganization. Disruption of EHD2 impairs caveolae-mediated endocytosis, alters membrane trafficking, and perturbs actin dynamics, leading to altered cell migration and signaling network rewiring.
In the AGS gastric cancer model, EHD2 knockout disrupts caveolar endocytosis and actin-mediated processes critical for tumor cell invasion and metastatic behavior. Because EHD2 is implicated in gastric cancer progression, its loss of function in this cell context allows direct examination of how endocytic trafficking impacts oncogenic signaling, cell motility, and drug sensitivity. Studies have suggested that altered EHD2 expression correlates with cancer aggressiveness; therefore, this polyclonal knockout model provides a physiologically relevant system to dissect the contributions of EHD2 to gastric adenocarcinoma pathophysiology.
This EHD2 polyclonal knockout cell population is suited for a range of advanced applications including western blotting, immunofluorescence localization studies, RNA sequencing to profile transcriptomic changes, and phospho-signaling analysis to map altered kinase networks. It enables functional assays such as wound-healing migration and Matrigel invasion to evaluate the role of EHD2 in gastric cancer cell motility. Additionally, the model can be used to assess drug resistance mechanisms linked to endocytic recycling and caveolar signaling. For further technical information or custom applications, please contact Ascent Research.
