The EEF1A2 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human ovarian adenocarcinoma cell line. This product delivers a loss-of-function model for the EEF1A2 gene, which encodes the eukaryotic translation elongation factor 1 alpha 2. The polyclonal format captures a heterogeneous pool of cells harboring target-gene disruptions, enabling robust population-level analyses without the bottleneck effects of clonal selection. It is intended for advanced biomedical research into the roles of EEF1A2 in translation, cytoskeletal organization, and apoptosis, and for translational cancer studies.
The MES-OV host cell line originates from the ascites of a patient with ovarian adenocarcinoma and represents an established epithelial model for studying ovarian cancer biology. These cells retain key oncogenic drivers and signaling networks, making them well-suited for investigating mechanisms of tumor cell proliferation, survival, migration, and drug resistance. The ovarian origin provides a clinically relevant context for evaluating the functional significance of genes implicated in ovarian malignancies, such as EEF1A2, which is frequently overexpressed in this cancer type.
EEF1A2 functions as a translation elongation factor that delivers aminoacyl-tRNAs to the ribosome, while also regulating actin cytoskeleton organization and inhibiting apoptosis. Its expression is positively regulated by the MYC proto-oncogene, EGF receptor signaling, heregulin, and STAT3, and is negatively modulated by miR-663 and miR-744. EEF1A2 promotes synthesis of pro-survival and proliferative proteins including CCND1, BCL2L1, PCNA, and MET. It interacts with the eEF1B complex (EEF1B2, EEF1D, EEF1G), actin (ACTB), HSP90AA1, AKT1, and PDPK1 (PDK1). Disruption of EEF1A2 impairs translation elongation and attenuates PI3K/Akt/mTOR signaling, which normally drives protein synthesis via effectors RPS6KB1 and EIF4EBP1.
Disruption of EEF1A2 in the MES-OV background is expected to impair oncogenic signaling by reducing the translation of critical proliferative and survival factors, thereby attenuating PI3K/Akt/mTOR pathway output and destabilizing the actin cytoskeleton. This polyclonal knockout model thus provides a powerful tool to dissect the specific contribution of translation elongation control to ovarian cancer cell fitness, apoptosis resistance, and motility. It enables researchers to link protein synthesis regulation directly to ovarian tumor phenotypes and to explore EEF1A2-dependent molecular networks.
These cells support a broad range of experimental applications, including functional investigation of EEF1A2 in ovarian cancer, identification of EEF1A2-regulated mRNAs through polysome profiling or RNA-seq, and mapping of protein interaction networks via co-immunoprecipitation. They can be employed in phenotypic assays such as viability (MTT), apoptosis (annexin V), and transwell migration, as well as in drug sensitivity screens to validate EEF1A2 as a therapeutic target. For further details or technical support, please contact Ascent Research.
