The EEF1A2 Knockout HGC-27 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human gastric carcinoma cell line HGC-27, featuring targeted disruption of the EEF1A2 gene. This loss-of-function model is generated using CRISPR/Cas9-mediated gene disruption, resulting in a heterogeneous pool of cells with EEF1A2 inactivation. As polyclonal cells, the product provides a representative knockout population suitable for batch-to-batch consistency in functional assays, without clonal isolation, and serves as a robust reagent for studying EEF1A2-dependent processes in gastric cancer.
HGC-27 is an epithelial cell line established from the lymph node metastasis of a gastric carcinoma patient. It exhibits an invasive, mesenchymal phenotype and is tumorigenic in vivo, making it a physiologically relevant model for gastric cancer progression and metastasis. The cells retain key oncogenic signaling pathways and are widely employed in gastrointestinal cancer research, particularly for investigating mechanisms of invasion, chemoresistance, and epithelial-mesenchymal transition (EMT). Their metastatic origin underscores their utility in studying advanced disease states, including cytoskeletal remodeling and translational dysregulation.
EEF1A2 encodes a eukaryotic translation elongation factor that facilitates the binding of aminoacyl-tRNA to the ribosome, thereby promoting protein synthesis. Beyond its canonical role in translation, EEF1A2 is implicated in cytoskeletal organization, apoptosis regulation, and signal transduction. In cancer, it is frequently overexpressed and functions downstream of EGFR, c-MYC, STAT3, HIF-1??, and PI3K/AKT signaling. Activated through the EGFR?CPI3K?CAKT?CmTOR?CS6K1 axis, EEF1A2 positively regulates the expression of proliferative and survival factors, including Cyclin D1 and Bcl-xL, and orchestrates ??-actin synthesis and vimentin upregulation, key determinants of EMT. EEF1A2 physically interacts with actin, the eEF1B complex, PAK4, and HSP90, forming a network that couples translational output to cytoskeletal dynamics.
In HGC-27 cells, EEF1A2 overexpression enhances proliferation and survival through upregulation of anti-apoptotic proteins and actin cytoskeleton reorganization, contributing to the aggressive phenotype of gastric cancer. The knockout model enables dissection of EEF1A2??s role in these processes, offering insight into how its loss attenuates PI3K/AKT/mTOR-driven oncogenic signaling, reduces Cyclin D1 and Bcl-xL abundance, and impairs migration and invasion. By disrupting this translation elongation hub, researchers can investigate the dependency of gastric carcinoma cells on EEF1A2 for maintaining the mesenchymal trait, chemoresistance, and tumorigenic potential in a polyclonal context that mimics tumor heterogeneity.
This product is suited for a wide range of advanced applications. Functional studies of EEF1A2 in gastric cancer can be performed using Western blotting to confirm knockout, RT-qPCR for mRNA quantitation, and proliferation (MTT/BrdU) or apoptosis (Annexin V) assays to assess phenotypic consequences. The model is amenable to drug screening targeting the translational elongation machinery, investigation of chemoresistance mechanisms, and exploration of cytoskeletal alterations in metastasis via Boyden chamber migration/invasion assays. Transcriptome- and translatome-wide analyses, including RNA-seq and polysome profiling, can uncover EEF1A2-dependent gene regulation. Immunofluorescence allows visualization of protein localization changes. For additional details or customized applications, please contact Ascent Research.
