The NME1 Knockout AGS Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal population derived from the AGS human gastric adenocarcinoma cell line, targeting the NME1 locus. This loss-of-function model provides a genetically heterogeneous pool of edited cells suitable for studying NME1-dependent processes without clonal selection. The polyclonal format helps capture functional diversity and reduces the risk of adaptation artifacts, while maintaining robust representation of the knockout phenotype across the population.
AGS cells are a well-characterized epithelial cell line established from a primary gastric adenocarcinoma, widely used to model gastric cancer biology, tumor microenvironment interactions, and drug response. These cells retain key features of gastric epithelium, including expression of adhesion molecules and responsiveness to growth factors, making them an appropriate host for investigating NME1 functions in a context that mirrors gastric epithelial malignancy. Their metastatic potential and signaling alterations render them particularly valuable for dissecting metastasis suppressor mechanisms.
NME1 encodes nucleoside diphosphate kinase A, a metastasis suppressor that inhibits cell migration and invasion. It directly binds KSR1 to negatively regulate Ras/ERK signaling, reducing ERK phosphorylation and downstream transcriptional programs. NME1 also modulates integrin-mediated adhesion and suppresses MMP-2 and MMP-9, limiting extracellular matrix degradation. Upstream, NME1 is transcriptionally regulated by TP53 and MYC, and its expression is silenced by DNA methylation and TGF-??. NME1 further interacts with STRAP, SET, and PRUNE, influencing Rho GTPase activity and cytoskeletal reorganization.
In the AGS gastric adenocarcinoma background, loss of NME1 function is expected to enhance migratory and invasive capacity, mirroring the aggressive phenotype observed in metastatic gastric cancer. This knockout model enables precise dissection of NME1??s role in suppressing epithelial-mesenchymal transition and maintaining cellular homeostasis. By disrupting NME1, researchers can interrogate how its absence alters downstream signaling through KSR1?CRas?CERK and RhoA?Cintegrin axes, providing a platform to study gastric cancer progression and identify vulnerabilities linked to NME1 loss.
This knockout model supports applications in metastasis suppression studies, gastric cancer invasion, and EMT research. Representative assays include wound-healing migration, transwell invasion, MTT/CCK-8 proliferation, Western blotting, RT-qPCR, phospho-ERK analysis, gelatin zymography, and co-immunoprecipitation. The cells are also suitable for drug resistance screening and integrin signaling studies. For further information, contact Ascent Research.
