The EHD3 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric carcinoma cell line, designed to disrupt the EHD3 gene. This product provides a heterogeneous pool of cells with targeted EHD3 loss-of-function, enabling researchers to investigate EHD3-dependent processes while preserving diverse genetic backgrounds and minimizing clonal selection artifacts. The polyclonal format reflects variable knockout efficiencies and maintains a more representative cellular context.
The HGC-27 cell line was established from a lymph node metastasis of a gastric adenocarcinoma patient, displaying epithelial morphology and retaining key malignant characteristics. It serves as a well-characterized model for gastric carcinoma research, recapitulating aspects of tumor proliferation, invasion, and metastatic potential. This background is especially relevant for examining the role of endocytic trafficking regulators in gastric cancer progression and for identifying novel therapeutic vulnerabilities.
EHD3 encodes an EPS15 homology domain-containing ATPase that localizes to endosomal compartments, where it functions as a key regulator of endocytic recycling. EHD3 interacts with a network of endocytic proteins, including EHD1, EHD2, syndapin, and Rab11-FIP2, to coordinate the trafficking of internalized receptors back to the plasma membrane. It is activated downstream of EGFR signaling and the PI3K/Akt pathway and controls the surface expression of critical receptors such as transferrin receptor (TFRC) and integrin ??1 (ITGB1). By modulating these receptors, EHD3 impacts cell adhesion, migration, and signal transduction. The Rab11-dependent recycling route and the actin cytoskeleton are integral components of the EHD3-associated membrane trafficking machinery.
In the context of HGC-27 gastric cancer cells, knockout of EHD3 disrupts the tightly regulated recycling of adhesion molecules and growth factor receptors, which can alter cellular behaviors central to tumorigenesis, including proliferation, migration, and invasion. This model may expose vulnerabilities in receptor trafficking that are essential for cancer cell survival and metastatic dissemination. Comparative analyses of wild-type and EHD3-knockout HGC-27 cells allow researchers to dissect the contribution of EHD3 to gastric cancer pathophysiology, explore its interplay with oncogenic signaling networks, and evaluate EHD3 as a potential therapeutic target in gastric adenocarcinoma and other EHD3-associated malignancies, such as breast cancer.
These polyclonal EHD3 knockout cells are suitable for a wide range of functional assays, including MTT proliferation assays, Transwell migration and invasion experiments, Western blotting, immunofluorescence microscopy, transferrin uptake assays, and apoptosis detection. Researchers can employ this model to investigate signaling pathways involving EGFR, Akt, and receptor recycling, assess drug responses in an EHD3-deficient background, or perform comparative proteomic and transcriptomic analyses. The product supports diverse studies in gastric cancer biology, endocytosis, and receptor trafficking. For further technical information, pricing, and customization options, please contact Ascent Research.
