Evidence map›Paper›PMID 24497838›Full record

ArticlePLoS genetics2014

Down-regulation of eIF4GII by miR-520c-3p represses diffuse large B cell lymphoma development.

Krystyna Mazan-Mamczarz, X Frank Zhao, Bojie Dai, James J Steinhardt, Raymond J Peroutka, Kimberly L Berk, Ari L Landon, Mariola Sadowska, Yongqing Zhang, Elin Lehrmann and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 49 citations in OpenAlex.

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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

14 authors at 4 institutions in 1 country.

Krystyna Mazan-MamczarzMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America.
X Frank ZhaoDepartment of Pathology, University of Maryland, Baltimore, Maryland, United States of America.
Bojie DaiMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America.
James J SteinhardtMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America.
Raymond J PeroutkaMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America.
Kimberly L BerkMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America.
Ari L LandonMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America.
Mariola SadowskaMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America.
Yongqing ZhangGene Expression and Genomics Unit, National Institute of Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Elin LehrmannGene Expression and Genomics Unit, National Institute of Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Kevin G BeckerGene Expression and Genomics Unit, National Institute of Aging, National Institutes of Health, Baltimore, Maryland, United States of America.
Rita ShaknovichPathology and Laboratory Medicine, Weill Cornell Medical College, New York, New York, United States of America.
Zhenqiu LiuMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America.
Ronald B GartenhausMarlene & Stewart Greenebaum Cancer Center, Department of Medicine, University of Maryland, Baltimore, Maryland, United States of America ; Veterans Administration Medical Center, Baltimore, Maryland, United States of America.
University of Maryland, Baltimore · USNational Institutes of Health · USCornell University · USInstitute on Aging · US

Funding

UCLA Clinical and Translational Science InstituteUL1TR000124 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DUBINETT, STEVEN M. · 2012 to 2015
$57.0M
UNIVERSITY OF MARYLAND GREENEBAUM CANCER CENTERSUPPORT GRANTP30CA134274 · NCI · UNIVERSITY OF MARYLAND BALTIMORE · PI FEYRUZ VIRGILIA RASSOOL · 2008 to 2026
$51.0M
Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
Alcohol Consumption and Risk of NHL: Role of MTOR DysfunctionR01AA017972 · NIAAA · UNIVERSITY OF MARYLAND BALTIMORE · PI GARTENHAUS, RONALD B · 2009 to 2013
$1.7M
MAP Kinase Signaling in Lymphoma: A Novel Therapeutic ParadigmR01CA164311 · NCI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI EVENS, ANDREW M, GARTENHAUS, RONALD B · 2012 to 2015
$1.4M
BLRD VA I01 BX002990Intramural NIH HHSNCATS NIH HHS UL1 TR000124NCI NIH HHS P30 CA134274NCI NIH HHS R01 CA164311NCI NIH HHS R01CA164311NIAAA NIH HHS R01 AA017972NIAAA NIH HHS R01AA017972
6 · The paper itself

Abstract

Deregulation of the translational machinery is emerging as a critical contributor to cancer development. The contribution of microRNAs in translational gene control has been established however; the role of microRNAs in disrupting the cap-dependent translation regulation complex has not been previously described. Here, we established that elevated miR-520c-3p represses global translation, cell proliferation and initiates premature senescence in HeLa and DLBCL cells. Moreover, we demonstrate that miR-520c-3p directly targets translation initiation factor, eIF4GII mRNA and negatively regulates eIF4GII protein synthesis. miR-520c-3p overexpression diminishes cells colony formation and reduces tumor growth in a human xenograft mouse model. Consequently, downregulation of eIF4GII by siRNA decreases translation, cell proliferation and ability to form colonies, as well as induces cellular senescence. In vitro and in vivo findings were further validated in patient samples; DLBCL primary cells demonstrated low miR-520c-3p levels with reciprocally up-regulated eIF4GII protein expression. Our results provide evidence that the tumor suppressor effect of miR-520c-3p is mediated through repression of translation while inducing senescence and that eIF4GII is a key effector of this anti-tumor activity.

Indexed as

Cell ProliferationAnimalsCell Line, TumorCellular SenescenceDown-RegulationEukaryotic Initiation Factor-4GGene Expression Regulation, NeoplasticHumansLymphoma, Large B-Cell, DiffuseMiceMicroRNAsRNA, MessengerRNA, Small InterferingUp-RegulationXenograft Model Antitumor AssaysEIF4G2 protein, humanEukaryotic Initiation Factor-4GMicroRNAsMIRN520 microRNA, humanRNA, MessengerRNA, Small Interfering

Identifiers

PMID24497838
PMCPMC3907297
OpenAlexW2092862044

What OpenQuestion holds

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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.