The EFNB1 Knockout HGC-27 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HGC-27 human gastric adenocarcinoma cell line, engineered for disruption of the EFNB1 gene. This product provides a heterogeneous pool of edited cells suitable for functional studies requiring loss-of-function models. The use of polyclonal knockout cells allows researchers to assess population-level effects of EFNB1 depletion without clonal selection, offering a more representative model of the genetic heterogeneity often observed in tumor biology.
The parental HGC-27 cell line was originally established from the lymph node metastasis of a gastric adenocarcinoma and serves as a well-characterized model for gastric cancer research. These cells exhibit features of aggressive, metastatic disease, including robust migratory and invasive properties. As a gastric adenocarcinoma line, HGC-27 is frequently employed in studies of tumor progression, metastasis, and signal transduction, making it a relevant host for investigating the role of EFNB1 in gastric cancer pathobiology.
EFNB1 encodes ephrin-B1, a transmembrane ligand for EphB receptor tyrosine kinases that mediates bidirectional cell-cell signaling. Ephrin-B1 engages EphB receptors to trigger forward signaling in the receptor-expressing cell and reverse signaling in the ligand-expressing cell, modulating cytoskeletal dynamics through Rho GTPases (RhoA, Rac1, Cdc42) and focal adhesion kinase (FAK). Downstream, Src and ERK1/2 transmit signals controlling adhesion, migration, and invasion. Upstream regulators include Wnt/??-catenin, p53, TGF-??, and hypoxia-induced HIF-1??. EFNB1 interacts with EphB receptors, Src, and PDZ adaptors such as GRIP and syntenin, integrating pathways that govern cell morphology and motility.
In gastric adenocarcinoma, EFNB1 dysregulation promotes tumor cell invasion and metastasis. The HGC-27 polyclonal knockout model allows dissection of ephrin-B1-dependent mechanisms in a cell background that natively expresses the ligand and its receptors. Abrogation of EFNB1 function enables evaluation of its role in epithelial-mesenchymal transition, directional migration, and tumor microenvironment interactions. This model is particularly suited for studying how loss of EFNB1 signaling affects Rho GTPase-driven cytoskeletal reorganization and downstream Src/FAK and MAPK/ERK cascade activation in gastric cancer.
Applications include transwell migration and invasion assays, phospho-signaling analysis of ERK and Src by Western blotting, immunofluorescence for adhesion proteins, and flow cytometry for Eph receptor expression. The cells are suitable for drug sensitivity screening, MTT viability assays, and xenograft tumor growth studies to assess EFNB1 in therapeutic response and in vivo progression. For additional information or custom editing inquiries, please contact Ascent Research.
