EEF-2 kinase: Another meddler in the "yin and yang" of Akt-mediated cell fate?

Yan Cheng, Li Yan, Xingcong Ren, Jin Ming Yang

Research output: Contribution to journalShort surveypeer-review

12 Scopus citations

Abstract

Eukaryotic elongation factor-2 (eEF-2) kinase, also known as calmodulindependent protein kinase III, is a unique calcium/calmodulin-dependent enzyme. eEF-2 kinase can act as a negative regulator of protein synthesis and a positive regulator of autophagy under environmental or metabolic stresses. Akt, a key downstream effector of the PI3K signaling pathway that regulates cell survival and proliferation, is an attractive therapeutic target for anticancer treatment. Akt inhibition leads to activation of both apoptosis, type I programmed cell death and autophagy, a cellular degradation process via lysosomal machinery (also termed type II programmed cell death). However, the underlying mechanisms that dictate functional relationship between autophagy and apoptosis in response to Akt inhibition remain to be delineated. Our recent study demonstrated that inhibition of eEF-2 kinase can suppress autophagy but promote apoptosis in tumor cells subjected to Akt inhibition, indicating a role of eEF-2 kinase as a controller in the crosstalk between autophagy and apoptosis. Furthermore, inhibition of eEF-2 kinase can reinforce the efficacy of a novel Akt inhibitor, MK-2206, against human glioma. These findings may help optimize the use of Akt inhibitors in the treatment of cancer and other diseases.

Original languageEnglish (US)
Pages (from-to)660-661
Number of pages2
JournalAutophagy
Volume7
Issue number6
DOIs
StatePublished - Jun 2011

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

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