The EEF1A2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line, carrying targeted disruptions in the EEF1A2 gene. This heterogeneous pool of cells provides a loss-of-function model for studying the role of the eukaryotic translation elongation factor 1 alpha 2 isoform. The polyclonal format minimizes clonal biases and is suitable for diverse functional assays in cancer research.
The AGS cell line, isolated from a human gastric adenocarcinoma, is an epithelial model widely used in gastric cancer studies. These cells retain epithelial barrier and secretory functions, and they respond to chemotherapeutic agents, providing a physiologically relevant context to investigate EEF1A2’s role in gastric tumorigenesis.
EEF1A2 encodes an isoform of eukaryotic elongation factor 1 alpha that delivers aminoacyl-tRNAs to the ribosome during protein synthesis. It also regulates the actin cytoskeleton and inhibits apoptosis. Upstream, EEF1A2 expression is driven by MYC, PI3K/AKT/mTOR, and MAPK/ERK signaling, which are commonly hyperactivated in cancer. Within the cell, EEF1A2 interacts with actin, the eEF1B complex, ribosomal proteins, valyl-tRNA synthetase, and ZPR1 to coordinate translation and cytoskeletal dynamics. Its downstream effects include enhanced global protein synthesis, actin remodeling, and suppression of apoptosis via Bcl-2 family proteins. Notably, EEF1A2 acts downstream of mTOR and 4E-BP1 in the PI3K/AKT/mTOR pathway, with its elongation activity modulated by eEF2 kinase.
In AGS gastric cancer cells, EEF1A2 promotes tumorigenesis by augmenting translation, remodeling the cytoskeleton, and inhibiting apoptosis. Knockout of EEF1A2 in this polyclonal population allows researchers to dissect its contributions to cell proliferation, survival, migration, and drug resistance, thereby validating it as a potential therapeutic target.
This model supports research in cancer biology, translational control, drug resistance, apoptosis, and cytoskeleton dynamics. Users can confirm knockout efficiency via western blotting and RT-qPCR, assess global translation using puromycin incorporation, and profile transcriptomes with RNA-seq. Phenotypic assays such as MTT proliferation, Annexin V apoptosis, and Transwell migration reveal functional impacts. Co-immunoprecipitation and immunofluorescence can detect altered protein complexes and actin architecture. Drug sensitivity testing with cisplatin and 5-FU evaluates chemoresistance. For further information or to discuss custom applications, please contact Ascent Research.
