Evidence map›Paper›PMID 25950472›Full record

ArticleCell death & disease2015

ErbB2-intronic microRNA-4728: a novel tumor suppressor and antagonist of oncogenic MAPK signaling.

D C Schmitt, L Madeira da Silva, W Zhang, Z Liu, R Arora, S Lim, A M Schuler, S McClellan, J F Andrews, A G Kahn and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

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  11. OncoTargets and therapy · 2020
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  18. Coamplification ofProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. Article
  20. Article
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

13 authors at 3 institutions in 2 countries.

D C SchmittDepartment of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA.
L Madeira da SilvaDepartment of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA.
W Zhang1] Department of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA [2] Department of Medical Laboratory Science, Xiangya School of Medicine, Central South University, Changsha 410013, China [3] Cancer Research Institute, Central South University, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha 410078, China.
Z LiuDepartment of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA.
R AroraDepartment of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA.
S LimDepartment of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA.
A M SchulerDepartment of Comparative Medicine, University of South Alabama, 307 N. University Blvd, Mobile, AL 36688, USA.
S McClellanDepartment of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA.
J F AndrewsDepartment of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA.
A G KahnDepartment of Pathology, University of South Alabama, 307 N. University Blvd, Mobile, AL 36688, USA.
M Zhou1] Cancer Research Institute, Central South University, Key Laboratory of Carcinogenesis, Ministry of Health, Key Laboratory of Carcinogenesis and Cancer Invasion, Ministry of Education, Changsha 410078, China [2] Hunan Cancer Hospital and the Affiliated Tumor Hospital of Xiang-Ya School of Medicine, Central South University, Changsha 410013, China.
E-Y E AhnDepartment of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA.
M Tan1] Department of Oncological Sciences, Mitchell Cancer Institute, University of South Alabama, 1600 Springhill Ave, Mobile, AL 36604, USA [2] Department of Biochemistry and Molecular Biology, University of South Alabama, 307 N. University Blvd, Mobile, AL 36688, USA.
University of South Alabama · USUSA Mitchell Cancer Institute · USCentral South University · CN

Funding

Glucose metabolism and ErbB2-mediated cancer progressionR01CA149646 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI TAN, MING · 2011 to 2016
$1.4M
NCI NIH HHS R01 CA149646NCI NIH HHS R01CA149646
6 · The paper itself

Abstract

Although the role of the ErbB2/HER2 oncogene in cancers has been extensively studied, how ErbB2 is regulated remains poorly understood. A novel microRNA, mir-4728, was recently found within an intron of the ErbB2 gene. However, the function and clinical relevance of this intronic miRNA are completely unknown. Here, we demonstrate that mir-4728 is a negative regulator of MAPK signaling through directly targeting the ERK upstream kinase MST4 and exerts numerous tumor-suppressive properties in vitro and in animal models. Importantly, our patient sample study shows that mir-4728 was under-expressed in breast tumors compared with normal tissue, and loss of mir-4728 correlated with worse overall patient survival. These results strongly suggest that mir-4728 is a tumor-suppressive miRNA that controls MAPK signaling through targeting MST4, revealing mir-4728's significance as a potential prognostic factor and target for therapeutic intervention in cancer. Moreover, this study represents a conceptual advance by providing strong evidence that a tumor-suppressive miRNA can antagonize the canonical signaling of its host oncogene.

Indexed as

Breast NeoplasmsCell Line, TumorCell ProliferationErb-b2 Receptor Tyrosine KinasesFemaleGene Expression Regulation, NeoplasticGenes, Tumor SuppressorHeLa CellsHumansIntronsMAP Kinase Signaling SystemMicroRNAsMitogen-Activated Protein Kinase KinasesSignal TransductionERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesMicroRNAsMIRN4728 microRNA, humanMitogen-Activated Protein Kinase Kinases

Identifiers

PMID25950472
PMCPMC4669696
OpenAlexW1588554328

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.