The EEF1A2 Knockout A-549 Polyclonal Cells product is a heterogeneous pool of human lung adenocarcinoma A-549 cells subjected to CRISPR/Cas9-mediated disruption of the EEF1A2 locus. This polyclonal knockout population provides a loss-of-function model for studying EEF1A2-dependent processes without clonal isolation artifacts.
The parental A-549 cell line, established from the lung adenocarcinoma of a 58-year-old male, exhibits an adherent epithelial morphology and a hypotriploid karyotype. It harbors an activating KRAS G12S mutation while retaining wild-type TP53, and is widely employed as a model for non-small cell lung cancer (NSCLC). A-549 cells retain features of alveolar type II pneumocytes, including expression of surfactant proteins, and are frequently utilized in studies of oncogenic signaling, apoptosis, and drug metabolism.
EEF1A2 encodes a GTP-dependent translation elongation factor that delivers aminoacyl-tRNA to the A-site of the ribosome, facilitating global protein synthesis. Beyond its canonical role in translation elongation, EEF1A2 promotes actin bundling and cytoskeletal organization through direct interactions with filamentous actin. In the A-549 context, EEF1A2 overexpression reinforces anti-apoptotic signaling by upregulating BCL-2 and BCL-xL, while its expression is positively regulated by transcription factors such as c-MYC and HIF-1??, and negatively modulated by the miR-221/222 microRNA cluster. The factor operates within a network including EEF1B2, EEF1D, phosphatidylinositol 4-kinase, and protein kinase C, linking translational control to cytoskeletal dynamics and survival pathways such as PI3K-AKT and MAPK/ERK.
Given A-549??s KRAS-driven oncogenic background, EEF1A2 knockout provides a relevant system to dissect the crosstalk between translation elongation and cancer cell viability. Loss of EEF1A2 function in these cells can reveal dependencies on enhanced translational output and actin-mediated motility, and may sensitize cells to apoptosis. This polyclonal knockout pool thus enables evaluation of EEF1A2 as a potential therapeutic target in lung adenocarcinoma and other malignancies with elevated EEF1A2 expression.
This EEF1A2 knockout product is suited for a variety of functional studies, including examination of translation elongation fidelity via puromycin incorporation assays and polysome profiling, assessment of cell proliferation (MTT assay), apoptosis (Annexin V staining), and migration (Transwell assay). Phalloidin staining can be used to visualize actin cytoskeletal changes, while western blotting and RT-qPCR verify target gene disruption and downstream effector expression. The model further supports drug screening campaigns aimed at identifying small molecules that exploit the loss of EEF1A2 to inhibit lung tumor growth. For additional information or custom inquiries, contact Ascent Research.
