The EHBP1 Knockout HGC-27 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population for loss-of-function studies of the EHBP1 gene in a human gastric cancer background. Derived from the HGC-27 gastric adenocarcinoma cell line, this polyclonal pool enables functional interrogation without clonal selection artifacts. CRISPR/Cas9-mediated genome editing generates a heterogeneous population of EHBP1-disrupted cells suitable for population-level phenotypic assays.
HGC-27 is a human gastric carcinoma cell line originally isolated from a lymph node metastasis of a gastric adenocarcinoma. As a model of aggressive gastric epithelial cancer, HGC-27 cells display deregulated migration and altered signal transduction, making them particularly relevant for investigating mechanisms underlying gastric cancer progression and metastasis.
EHBP1 encodes an endocytic adaptor protein that bridges clathrin-mediated endocytosis with the actin cytoskeleton. It interacts with EHD1, EHD2, F-actin, clathrin, and the AP-2 adaptor complex to regulate vesicle formation, scission, and recycling. Downstream of EGFR and receptor tyrosine kinase signaling, EHBP1 integrates membrane tension to coordinate actin polymerization at endocytic sites. By modulating trafficking and surface presentation of critical receptors, EHBP1 influences signaling cascades governing cell adhesion, migration, and proliferation.
In the HGC-27 gastric cancer model, EHBP1 disruption is anticipated to impair endocytic recycling and alter spatial dynamics of surface receptors such as EGFR. Given the role of endocytic trafficking in tumor invasion and metastasis, perturbation of EHBP1-mediated processes may attenuate the migratory and invasive capacity of gastric carcinoma cells. This knockout model thus provides a powerful tool for dissecting how endocytic adaptors contribute to the malignant phenotype, potentially revealing therapeutic vulnerabilities in the endocytic machinery.
Researchers can apply this polyclonal knockout cell population to a wide range of experiments. Western blotting and RT-qPCR confirm EHBP1 disruption; immunofluorescence co-staining for EHBP1 and F-actin or EHD1 visualizes endocytic organization. Functional assays??flow cytometry for EGFR internalization, transwell migration/invasion, and phospho-signaling analysis??enable detailed characterization. Co-immunoprecipitation probes impaired EHBP1-EHD interactions. Applications include EGFR trafficking, actin dynamics, drug resistance, and endocytosis in gastric cancer. For further information, contact Ascent Research.
