Evidence map›Paper›PMID 24698324›Full record

ArticleThe Journal of allergy and clinical immunology2014

MicroRNA-150 regulates the cytotoxicity of natural killers by targeting perforin-1.

Nayoung Kim, Miju Kim, Sohyun Yun, Junsang Doh, Philip D Greenberg, Tae-Don Kim, Inpyo Choi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of allergy and clinical immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.9field-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

47 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
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  7. Plasma exosomal miR-150-3p,American journal of cancer research · 2025
    Article
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  16. MicroRNA-regulated B cells in obesity.Immunometabolism (Cobham, Surrey) · 2022
    Review
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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

7 authors at 4 institutions in 2 countries.

Nayoung KimImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea.
Miju KimSchool of Interdisciplinary Bioscience and Bioengineering (I-Bio), POSTECH, Pohang, Korea; Department of Mechanical Engineering, POSTECH, Pohang, Korea.
Sohyun YunImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea.
Junsang DohSchool of Interdisciplinary Bioscience and Bioengineering (I-Bio), POSTECH, Pohang, Korea; Department of Mechanical Engineering, POSTECH, Pohang, Korea.
Philip D GreenbergDepartments of Immunology and Medicine, University of Washington School of Medicine, and Fred Hutchinson Cancer Research Center, Seattle, Wash.
Tae-Don KimImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea; Department of Functional Genomics, University of Science and Technology (UST), KRIBB, Daejeon, Korea. Electronic address: tdkim@kribb.re.kr.
Inpyo ChoiImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Korea; Department of Functional Genomics, University of Science and Technology (UST), KRIBB, Daejeon, Korea. Electronic address: ipchoi@kribb.re.kr.
Korea Research Institute of Bioscience and Biotechnology · KRKorea University of Science and Technology · KRPohang University of Science and Technology · KRFred Hutch Cancer Center · US

Funding

Mechanisms of Murine Turmor Eradication by ImmunotherapyR01CA033084 · NCI · UNIVERSITY OF WASHINGTON · PI GREENBERG, PHILIP D · 1986 to 2017
$5.8M
MECHANISMS OF MURINE TUMOR ERADICATION BY IMMUNOTHERAPYR37CA033084 · NCI · UNIVERSITY OF WASHINGTON · PI GREENBERG, PHILIP D · 1991 to 2006
$3.5M
NCI NIH HHS CA33084NCI NIH HHS R01 CA033084NCI NIH HHS R37 CA033084
6 · The paper itself

Abstract

backgroundPerforin-1 (Prf1) is the predominant cytolytic protein secreted by natural killer (NK) cells. For a rapid immune response, resting NK cells contain high Prf1 mRNA concentrations while exhibiting minimal cytotoxicity caused by a blockage of Prf1 protein synthesis, implying that an unknown posttranscriptional regulatory mechanism exists.

objectiveWe sought to determine whether microRNA-150 (miR-150) posttranscriptionally regulates Prf1 translation in both mouse and human NK cells at rest and at various time points after activation.

methodsMouse NK cells with a targeted deletion of miR-150 (miR-150(-/-) NK cells), primary human NK cells, and NK92 MI cells were used to investigate the role of miR-150 in NK cells. NK cell cytotoxicity assays and Western blotting proved that activated miR-150(-/-) NK cells expressed upregulated Prf1, augmenting NK cell cytotoxicity. When immunodeficient mice were injected with miR-150(-/-) NK cells, there was a significant reduction in tumor growth and metastasis of B16F10 melanoma.

resultsWe report that miR-150 binds to 3' untranslated regions of mouse and human Prf1, posttranscriptionally downregulating its expression. Mouse wild-type NK cells displayed downregulated miR-150 expression in response to IL-15, which led to corresponding repression and induction of Prf1 during rest and after IL-15 activation, respectively.

conclusionOur results indicate that miR-150 is a common posttranscriptional regulator for Prf1 in mouse and human NK cells that represses NK cell lytic activity. Thus the therapeutic control of miR-150 in NK cells could enhance NK cell-based immunotherapy against cancer, providing a better clinical outcome.

Indexed as

3' Untranslated RegionsAnimalsBinding SitesCells, CulturedCytotoxicity, ImmunologicGene Expression RegulationHumansInterleukin-15Killer Cells, NaturalMelanoma, ExperimentalMiceMicroRNAsPerforinPore Forming Cytotoxic ProteinsProtein BiosynthesisSignal Transduction3' Untranslated RegionsInterleukin-15MicroRNAsMIR150, humanMirn150 microRNA, mousePerforinperforin 1, mousePore Forming Cytotoxic ProteinsPRF1 protein, humanimmunotherapymiR-150NK cell cytotoxicityNK cellsperforin-1post-transcriptional regulationtumor growth and metastasis

Identifiers

PMID24698324
PMCPMC4125537
OpenAlexW2129621430

What OpenQuestion holds

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LicenceTDM
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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.