The EEF2K Knockout MES-OV Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population generated on the MES-OV human ovarian clear cell carcinoma cell line. This product provides a heterogeneous loss-of-function model in which the EEF2K gene, encoding eukaryotic elongation factor 2 kinase, has been disrupted across a cell population. By using a polyclonal format, the cells avoid clonal selection artifacts and capture diverse gene editing outcomes, making the population suitable for pooled screening and robust population-level analyses of translational control in ovarian cancer.
MES-OV is an established epithelial ovarian cancer cell line derived from an ovarian clear cell carcinoma, a distinct histological subtype characterized by unique molecular pathology and clinical behavior. This line faithfully retains key features of clear cell carcinoma, including relevant oncogenic signaling networks, and serves as a widely used in vitro model for studying disease mechanisms, therapeutic response, and drug resistance. Combining EEF2K disruption with this host line allows targeted investigation of the kinase’s function specifically within the ovarian clear cell carcinoma context.
EEF2K is a calcium/calmodulin-dependent serine/threonine kinase that directly phosphorylates eukaryotic elongation factor 2 (eEF2) at Thr56, reducing its ribosomal affinity and thereby inhibiting translation elongation to suppress global protein synthesis. Its activity is regulated by multiple upstream pathways: it is activated by calmodulin in response to intracellular calcium and by AMPK under energy stress, while mTORC1 and PKA phosphorylate inhibitory sites to relieve translational suppression under growth-promoting conditions. Downstream targets include eEF2, the protein synthesis machinery, BDNF translation, and cell cycle regulators. Thus, EEF2K integrates signals from calcium, energy status, and growth factors to dynamically tune translation rates.
In ovarian clear cell carcinoma, EEF2K may contribute to metabolic adaptation and chemoresistance by modulating protein synthesis during stress. This knockout model enables direct dissection of how loss of EEF2K-dependent translational control affects proliferation, apoptosis, and sensitivity to standard chemotherapies such as platinum agents. It also allows examination of cross-talk among mTORC1, AMPK, and calcium signaling in an endogenous ovarian cancer background, offering insights into potential vulnerabilities that could be exploited therapeutically.
Typical applications include western blotting for phospho-EEF2K and phospho-eEF2 to confirm pathway disruption, polysome profiling and puromycin incorporation assays to measure translation elongation rates, RT-qPCR for downstream gene expression changes, and MTT or apoptosis assays under metabolic or chemotherapeutic stress. The model supports studies of translational reprogramming, drug resistance, and synthetic lethality in ovarian cancer. For more information or to request a quote, please contact Ascent Research.
