Evidence map›Paper›PMID 24955726›Full record

ArticleAutophagy2014

Silencing of EEF2K (eukaryotic elongation factor-2 kinase) reveals AMPK-ULK1-dependent autophagy in colon cancer cells.

Chuan-Ming Xie, Xiao-Yu Liu, Kathy W Y Sham, Josie M Y Lai, Christopher H K Cheng

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.1field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
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  4. Review
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    Article
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  15. Review
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  18. Frontiers in pharmacology · 2022
    Article
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  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 2 countries.

Chuan-Ming XieSchool of Biomedical Sciences; The Chinese University of Hong Kong; Hong Kong, China.
Xiao-Yu LiuSchool of Biomedical Sciences; The Chinese University of Hong Kong; Hong Kong, China.
Kathy W Y ShamSchool of Biomedical Sciences; The Chinese University of Hong Kong; Hong Kong, China.
Josie M Y LaiSchool of Biomedical Sciences; The Chinese University of Hong Kong; Hong Kong, China.
Christopher H K ChengSchool of Biomedical Sciences; The Chinese University of Hong Kong; Hong Kong, China; Center of Novel Functional Molecules; The Chinese University of Hong Kong; Hong Kong, China.
Chinese University of Hong Kong · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

EEF2K (eukaryotic elongation factor-2 kinase), also known as Ca (2+)/calmodulin-dependent protein kinase III, functions in downregulating peptide chain elongation through inactivation of EEF2 (eukaryotic translation elongation factor 2). Currently, there is a limited amount of information on the promotion of autophagic survival by EEF2K in breast and glioblastoma cell lines. However, the precise role of EEF2K in carcinogenesis as well as the underlying mechanism involved is still poorly understood. In this study, contrary to the reported autophagy-promoting activity of EEF2K in certain cancer cells, EEF2K is shown to negatively regulate autophagy in human colon cancer cells as indicated by the increase of LC3-II levels, the accumulation of LC3 dots per cell, and the promotion of autophagic flux in EEF2K knockdown cells. EEF2K negatively regulates cell viability, clonogenicity, cell proliferation, and cell size in colon cancer cells. Autophagy induced by EEF2K silencing promotes cell survival and does not potentiate the anticancer efficacy of the AKT inhibitor MK-2206. In addition, autophagy induced by silencing of EEF2K is attributed to induction of protein synthesis and activation of the AMPK-ULK1 pathway, independent of the suppression of MTOR activity and ROS generation. Knockdown of AMPK or ULK1 significantly abrogates EEF2K silencing-induced increase of LC3-II levels, accumulation of LC3 dots per cell as well as cell proliferation in colon cancer cells. In conclusion, silencing of EEF2K promotes autophagic survival via activation of the AMPK-ULK1 pathway in colon cancer cells. This finding suggests that upregulation of EEF2K activity may constitute a novel approach for the treatment of human colon cancer.

Indexed as

AMP-Activated Protein KinasesAutophagyAutophagy-Related Protein-1 HomologCell Line, TumorCell ProliferationCell SurvivalColonic NeoplasmsElongation Factor 2 KinaseGene SilencingHeterocyclic Compounds, 3-RingHumansIntracellular Signaling Peptides and ProteinsProtein Serine-Threonine KinasesSignal TransductionAMP-Activated Protein KinasesAutophagy-Related Protein-1 HomologElongation Factor 2 KinaseHeterocyclic Compounds, 3-RingIntracellular Signaling Peptides and ProteinsMK 2206Protein Serine-Threonine KinasesULK1 protein, humanAMPKATGautophagycancer growthcell survivalcolon cancerelongation factor-2 kinaseMTORROSULK1

Identifiers

PMID24955726
PMCPMC4206530
OpenAlexW2015136946

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.