The EHBP1 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the EHBP1 gene has been disrupted in the AGS human gastric adenocarcinoma cell line. This pooled format preserves genetic diversity and avoids clonal bias, providing a robust loss-of-function model for studying EHBP1-dependent phenotypes in a physiologically relevant epithelial context.
The AGS cell line is derived from a gastric adenocarcinoma and serves as a widely used in vitro model for gastric cancer research, including studies on Helicobacter pylori infection, signal transduction, and metastatic behavior. These epithelial cells exhibit intrinsic migratory and invasive capabilities, making them an ideal host for dissecting the contributions of EHBP1 to actin-dependent processes that underpin tumor progression.
EHBP1 encodes an actin-binding adaptor that links EH-domain-containing proteins EHD1 and EHD2 on endocytic vesicles to the actin cytoskeleton, directly interacting with clathrin and the AP-2 complex to regulate clathrin-mediated endocytosis. Upstream, EHBP1 is influenced by epidermal growth factor receptor (EGFR) signaling, the small GTPase Rab5, and the PI3K/AKT pathway. Downstream, it orchestrates actin dynamics, endocytic trafficking, and the assembly of cell migration machinery, thereby integrating membrane traffic with cytoskeletal remodeling.
Disruption of EHBP1 in AGS cells impairs clathrin-mediated endocytosis and compromises actin-dependent functions, notably reducing cell migration and invasion. This knockout model thus enables detailed investigation of how endocytic trafficking feeds into gastric cancer cell motility and metastatic potential, and how loss of EHBP1 alters signal integration downstream of growth factor receptors and small GTPases.
Applications include transferrin uptake assays to measure endocytosis, transwell migration and invasion assays to quantify motility, co-immunoprecipitation to analyze protein complex integrity, and immunofluorescence to visualize actin cytoskeleton alterations. Western blotting confirms EHBP1 depletion, while phospho-signaling analyses (e.g., EGFR, AKT) reveal changes in pathway activation. This tool supports research on endocytosis, tumor cell migration, and EHBP1 as a therapeutic target in gastric cancer. For further details, please contact Ascent Research.
