EGFR Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line, carrying a targeted disruption of the EGFR gene. This heterogeneous loss-of-function model avoids clonal selection artifacts, making it suitable for robust, population-level studies of EGFR signaling.
The AGS cell line was established from a human gastric adenocarcinoma and displays a transformed epithelial phenotype with anchorage-independent growth. As a widely used gastric cancer model, AGS cells facilitate investigation of oncogenic pathways, drug sensitivity, and metastasis, where EGFR-mediated signaling is frequently upregulated.
EGFR encodes a receptor tyrosine kinase activated by ligands such as EGF, TGF-alpha, amphiregulin, and epiregulin, leading to receptor dimerization and autophosphorylation. This recruits adaptors including GRB2, SHC, and CBL, which couple to SOS and activate the RAS-RAF1-MAP2K1-MAPK1 (ERK) cascade. Concurrently, EGFR engages the PI3KCA-AKT1-MTOR axis and can crosstalk with JAK/STAT signaling. Key downstream transcriptional targets include FOS, JUN, MYC, CCND1, and BIRC5, driving cell cycle progression and anti-apoptotic programs. EGFR also forms heterodimers with ERBB2 and ERBB3, broadening signal diversity.
Disruption of EGFR in AGS cells eliminates ligand-induced activation of MAPK/ERK and PI3K/AKT cascades, thereby reducing proliferation and survival signals essential for the malignant phenotype. This knockout model holds particular relevance for gastric cancer research, where EGFR amplification occurs, and for preclinical evaluation of EGFR inhibitors used in non-small cell lung cancer, colorectal, and head and neck cancers.
These polyclonal knockout cells support a range of assays, including western blotting for EGFR protein, RT-qPCR for mRNA, and phospho-EGFR ELISA to quantify pathway inactivation. Proliferation and migration assays can reveal EGFR-dependent growth and motility, while drug sensitivity profiling with tyrosine kinase inhibitors (e.g., gefitinib, erlotinib) helps dissect on-target effects and resistance mechanisms. They also provide a clean background for re-expression studies to validate EGFR variants. For further details or to obtain a quote, please contact Ascent Research.
