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 survey

12 Citations (Scopus)

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 - Jan 1 2011

Fingerprint

Yin-Yang
Elongation Factor 2 Kinase
Autophagy
Phosphotransferases
Apoptosis
Physiological Stress
Calmodulin
Phosphatidylinositol 3-Kinases
Glioma
Neoplasms
Cell Survival
Therapeutics
Cell Proliferation
Calcium
Enzymes

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cell Biology

Cite this

Cheng, Yan ; Yan, Li ; Ren, Xingcong ; Yang, Jin-Ming. / EEF-2 kinase : Another meddler in the "yin and yang" of Akt-mediated cell fate?. In: Autophagy. 2011 ; Vol. 7, No. 6. pp. 660-661.
@article{23e2072e310842bba155f9728d58dd15,
title = "EEF-2 kinase: Another meddler in the {"}yin and yang{"} of Akt-mediated cell fate?",
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.",
author = "Yan Cheng and Li Yan and Xingcong Ren and Jin-Ming Yang",
year = "2011",
month = "1",
day = "1",
doi = "10.4161/auto.7.6.15385",
language = "English (US)",
volume = "7",
pages = "660--661",
journal = "Autophagy",
issn = "1554-8627",
publisher = "Landes Bioscience",
number = "6",

}

EEF-2 kinase : Another meddler in the "yin and yang" of Akt-mediated cell fate? / Cheng, Yan; Yan, Li; Ren, Xingcong; Yang, Jin-Ming.

In: Autophagy, Vol. 7, No. 6, 01.01.2011, p. 660-661.

Research output: Contribution to journalShort survey

TY - JOUR

T1 - EEF-2 kinase

T2 - Another meddler in the "yin and yang" of Akt-mediated cell fate?

AU - Cheng, Yan

AU - Yan, Li

AU - Ren, Xingcong

AU - Yang, Jin-Ming

PY - 2011/1/1

Y1 - 2011/1/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=79957881198&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79957881198&partnerID=8YFLogxK

U2 - 10.4161/auto.7.6.15385

DO - 10.4161/auto.7.6.15385

M3 - Short survey

C2 - 21460616

AN - SCOPUS:79957881198

VL - 7

SP - 660

EP - 661

JO - Autophagy

JF - Autophagy

SN - 1554-8627

IS - 6

ER -