ArticleCellular signalling2016
Elongation factor 2 kinase promotes cell survival by inhibiting protein synthesis without inducing autophagy.
Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Targeted Degradation of eEF2K by a Structure-Guided PROTAC Strategy for the Treatment of Triple-Negative Breast Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Decreased tRNA abundance contributes to decreased translation elongation rate in a prolonged mitosis.bioRxiv : the preprint server for biology · 2026Article
- Towards a cleaner CHO chassis: systematic knockout of host cell proteins for efficient biopharmaceutical manufacturing.Frontiers in bioengineering and biotechnology · 2026Article
- eEF2K is a poor prognostic factor and novel molecular target in pancreatic cancer: regulating tumor growth and progression via the tumor microenvironment.Cell death & disease · 2025Article
- Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans.Nature communications · 2025Article
- Targeting glutamine dependence with DRP-104 inhibits proliferation and tumor growth of castration-resistant prostate cancer.The Prostate · 2024Article
- MicroRNAs as the critical regulators of Forkhead box protein family during gynecological and breast tumor progression and metastasis.European journal of medical research · 2023Review
- Ghrelin rapidly elevates protein synthesis in vitro by employing the rpS6K-eEF2K-eEF2 signalling axis.Cellular and molecular life sciences : CMLS · 2022Article
- Formation and persistence of polyglutamine aggregates in mistranslating cells.Nucleic acids research · 2021Article
- Autophagy inhibition and microRNA‑199a‑5p upregulation in paclitaxel‑resistant A549/T lung cancer cells.Oncology reports · 2021Article
- Progress in the Development of Eukaryotic Elongation Factor 2 Kinase (eEF2K) Natural Product and Synthetic Small Molecule Inhibitors for Cancer Chemotherapy.International journal of molecular sciences · 2021Review
- Insights Into the Pathologic Roles and Regulation of Eukaryotic Elongation Factor-2 Kinase.Frontiers in molecular biosciences · 2021Review
- Article
- Cunning maneuver regulating chemotherapy resistance in triple-negative breast cancer by eEF2K and autophagy.Annals of translational medicine · 2020Article
- Eukaryotic elongation factor-2 kinase (eEF2K) signaling in tumor and microenvironment as a novel molecular target.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Treatment response in triple-negative breast cancer: a role for eEF2 kinase-mediated autophagy?Annals of translational medicine · 2020Article
- The eEF2 kinase-induced STAT3 inactivation inhibits lung cancer cell proliferation by phosphorylation of PKM2.Cell communication and signaling : CCS · 2020Article
- eEF2 kinase mediated autophagy as a potential therapeutic target for paclitaxel-resistant triple-negative breast cancer.Annals of translational medicine · 2019Article
- Eukaryotic elongation factor-2 kinase expression is an independent prognostic factor in colorectal cancer.BMC cancer · 2019Article
- Cross-talk between protein synthesis, energy metabolism and autophagy in cancer.Current opinion in genetics & development · 2018Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
Abstract
Eukaryotic elongation factor 2 kinase (eEF2K) inhibits the elongation stage of protein synthesis by phosphorylating its only known substrate, eEF2. eEF2K is tightly regulated by nutrient-sensitive signalling pathways. For example, it is inhibited by signalling through mammalian target of rapamycin complex 1 (mTORC1). It is therefore activated under conditions of nutrient deficiency. Here we show that inhibiting eEF2K or knocking down its expression renders cancer cells sensitive to death under nutrient-starved conditions, and that this is rescued by compounds that block protein synthesis. This implies that eEF2K protects nutrient-deprived cells by inhibiting protein synthesis. Cells in which signalling through mTORC1 is highly active are very sensitive to nutrient withdrawal. Inhibiting mTORC1 protects them. Our data reveal that eEF2K makes a substantial contribution to the cytoprotective effect of mTORC1 inhibition. eEF2K is also reported to promote another potentially cytoprotective process, autophagy. We have used several approaches to test whether inhibition or loss of eEF2K affects autophagy under a variety of conditions. We find no evidence that eEF2K is involved in the activation of autophagy in the cell types we have studied. We conclude that eEF2K protects cancer cells against nutrient starvation by inhibiting protein synthesis rather than by activating autophagy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.