Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/111966
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Type: Journal article
Title: Eukaryotic elongation factor 2 kinase (eEF2K) in cancer
Author: Wang, X.
Xie, J.
Proud, C.
Citation: Cancers, 2017; 9(12):162-1-162-15
Publisher: MDPI AG
Issue Date: 2017
ISSN: 2072-6694
2072-6694
Statement of
Responsibility: 
Xuemin Wang, Jianling Xie and Christopher G. Proud
Abstract: Eukaryotic elongation factor 2 kinase (eEF2K) is a highly unusual protein kinase that negatively regulates the elongation step of protein synthesis. This step uses the vast majority of the large amount of energy and amino acids required for protein synthesis. eEF2K activity is controlled by an array of regulatory inputs, including inhibition by signalling through mammalian target of rapamycin complex 1 (mTORC1). eEF2K is activated under conditions of stress, such as energy depletion or nutrient deprivation, which can arise in poorly-vascularised tumours. In many such stress conditions, eEF2K exerts cytoprotective effects. A growing body of data indicates eEF2K aids the growth of solid tumours in vivo. Since eEF2K is not essential (in mice) under ‘normal’ conditions, eEF2K may be a useful target in the treatment of solid tumours. However, some reports suggest that eEF2K may actually impair tumorigenesis in some situations. Such a dual role of eEF2K in cancer would be analogous to the situation for other pathways involved in cell metabolism, such as autophagy and mTORC1. Further studies are needed to define the role of eEF2K in different tumour types and at differing stages in tumorigenesis, and to assess its utility as a therapeutic target in oncology.
Keywords: mRNA translation; mTORC1; AMPK; eEF2; autophagy; migration; α-kinase
Description: Published: 27 November 2017
Rights: © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
RMID: 0030079331
DOI: 10.3390/cancers9120162
Appears in Collections:Molecular and Biomedical Science publications

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