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The eEF2 kinase-induced STAT3 inactivation inhibits lung cancer cell proliferation by phosphorylation of PKM2

Overview of attention for article published in Cell Communication and Signaling, February 2020
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Title
The eEF2 kinase-induced STAT3 inactivation inhibits lung cancer cell proliferation by phosphorylation of PKM2
Published in
Cell Communication and Signaling, February 2020
DOI 10.1186/s12964-020-0528-y
Pubmed ID
Authors

Min Xiao, Jianling Xie, Yu Wu, Genzhu Wang, Xin Qi, Zailiang Liu, Yuying Wang, Xuemin Wang, Ashfaqul Hoque, Jon Oakhill, Christopher G. Proud, Jing Li

Abstract

Eukaryotic elongation factor-2 kinase (eEF2K) is a Ca 2+ /calmodulin (CaM)-dependent protein kinase that inhibits protein synthesis. However, the role of eEF2K in cancer development was reported paradoxically and remains to be elucidated. Herein, A549 cells with eEF2K depletion or overexpression by stably transfected lentivirus plasmids were used in vitro and in vivo study. MTT and colony assays were used to detect cell proliferation and growth. Extracellular glucose and lactate concentration were measured using test kit. Immunoblot and co-immunoprecipitation assays were used to examine the molecular biology changes and molecular interaction in these cells. LC-MS/MS analysis and [γ- 32 P] ATP kinase assay were used to identify combining protein and phosphorylation site. Nude mice was utilized to study the correlation of eEF2K and tumor growth in vivo. We demonstrated that eEF2K inhibited lung cancer cells proliferation and affected the inhibitory effects of EGFR inhibitor gefitinib. Mechanistically, we showed that eEF2K formed a complex with PKM2 and STAT3, thereby phosphorylated PKM2 at T129, leading to reduced dimerization of PKM2. Subsequently, PKM2 impeded STAT3 phosphorylation and STAT3-dependent c-Myc expression. eEF2K depletion promoted the nuclear translocation of PKM2 and increased aerobic glycolysis reflected by increased lactate secretion and glucose. Our findings define a novel mechanism underlying the regulation of cancer cell proliferation by eEF2K independent of its role in protein synthesis, disclosing the diverse roles of eEF2K in cell biology, which lays foundation for the development of new anticancer therapeutic strategies.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 25 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 25 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 4 16%
Student > Master 3 12%
Researcher 3 12%
Student > Ph. D. Student 1 4%
Other 1 4%
Other 2 8%
Unknown 11 44%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 4 16%
Pharmacology, Toxicology and Pharmaceutical Science 2 8%
Medicine and Dentistry 2 8%
Social Sciences 1 4%
Neuroscience 1 4%
Other 1 4%
Unknown 14 56%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 14 February 2020.
All research outputs
#20,714,793
of 23,314,015 outputs
Outputs from Cell Communication and Signaling
#963
of 1,040 outputs
Outputs of similar age
#383,413
of 457,645 outputs
Outputs of similar age from Cell Communication and Signaling
#46
of 46 outputs
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So far Altmetric has tracked 1,040 research outputs from this source. They receive a mean Attention Score of 3.9. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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We're also able to compare this research output to 46 others from the same source and published within six weeks on either side of this one. This one is in the 1st percentile – i.e., 1% of its contemporaries scored the same or lower than it.