The ADAM10 Knockout AGS Polyclonal Cells constitute a CRISPR/Cas9?mediated gene?disrupted polyclonal cell population derived from the AGS human gastric adenocarcinoma line. This product offers a pooled knockout model in which ADAM10 function is abolished across a heterogeneous cell population, avoiding clonal artifacts while maintaining biologically relevant diversity. The polyclonal format is particularly advantageous for studies requiring robust, reproducible loss?of?function phenotypes in a cancer?relevant background.
The AGS cell line was established from the gastric adenocarcinoma of a 54?year?old female and serves as a widely used epithelial model for gastric cancer research. It displays adherent growth and retains key signaling pathways, making it a suitable host for investigating ADAM10?dependent mechanisms in gastric tumorigenesis, metastasis, and therapeutic response.
ADAM10 is a transmembrane metalloprotease responsible for ectodomain shedding of multiple substrates, including NOTCH1, NOTCH2, E?cadherin, HB?EGF, TNF??, and APP. Its activity is regulated by Notch ligands (JAG1, DLL1), EGF, PMA, and calcium influx, and it interacts with tetraspanin partners TSPAN12, TSPAN14, and TSPAN33. Downstream, cleaved NOTCH1 intracellular domain translocates to the nucleus to activate transcription of HES1, while shed HB?EGF engages EGFR to trigger MAPK1/3 phosphorylation, and soluble E?cadherin fragments modulate cell adhesion dynamics.
Knockout of ADAM10 in AGS cells disrupts these signaling networks, leading to diminished Notch pathway activity, reduced EGFR?driven proliferation, and altered cadherin?mediated cell adhesion, collectively impairing tumorigenic potential and metastatic capacity. This model is thus valuable for studying gastric cancer progression, validating ADAM10 as a therapeutic target, and exploring its roles in Alzheimer??s disease and inflammatory conditions through altered APP and CX3CL1 processing.
Researchers can apply this knockout model in a range of assays including Western blotting and RT?qPCR for expression analysis, flow cytometry and immunofluorescence for phenotypic characterization, and functional studies such as transwell migration/invasion, cell viability, and xenograft tumor growth in immunodeficient mice. It is particularly suited for drug?target validation of ADAM10 inhibitors, Notch reporter luciferase assays, and apoptosis/proliferation studies. For further information, please contact Ascent Research.
