Evidence map›Paper›PMID 31406207›Full record

ArticleScientific reports2019

Exosomal miR-16-5p as a target for malignant mesothelioma.

Phillip B Munson, Elizabeth M Hall, Nicholas H Farina, Harvey I Pass, Arti Shukla

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

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.0field-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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 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

5 authors at 2 institutions in 1 country.

Phillip B MunsonDepartment of Pathology and Laboratory Medicine, University of Vermont, College of Medicine, Burlington, VT, 05405, USA.
Elizabeth M HallDepartment of Pathology and Laboratory Medicine, University of Vermont, College of Medicine, Burlington, VT, 05405, USA.
Nicholas H FarinaDepartment of Biochemistry, University of Vermont, College of Medicine, Burlington, VT, 05405, USA.
Harvey I PassDepartment of Cardiothoracic Surgery, NYU Langone Medical Center, 530 First Avenue, 9V New York, New York, 10016, USA.
Arti ShuklaDepartment of Pathology and Laboratory Medicine, University of Vermont, College of Medicine, Burlington, VT, 05405, USA. Arti.Shukla@med.uvm.edu.
University of Vermont · USNYU Langone Health · US

Funding

Inflammasomes in pathogenesis of mesotheliomaR01ES021110 · NIEHS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI SHUKLA, ARTI · 2012 to 2016
$1.7M
Nikon A1R-ER Confocal Microscope for the Microscopy Imaging CenterS10OD025030 · OD · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI TAATJES, DOUGLAS J. · 2018 to 2018
$557k
Unfolded protein responses in carbon nanotube-induced mesothelial cell fibrosis and mesotheliomaR21ES028857 · NIEHS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI SHUKLA, ARTI · 2018 to 2019
$429k
NIEHS NIH HHS R01 ES021110NIEHS NIH HHS R21 ES028857NIH HHS S10 OD025030
6 · The paper itself

Abstract

Malignant mesothelioma (MM) is an asbestos-induced cancer arising on the mesothelial surface of organ cavities. MM is essentially incurable without a means of early diagnosis and no successful standard of care. These facts indicate a deep chasm of knowledge that needs to be filled. Our group recently delved into MM tumor biology from the perspective of exosome-contained microRNAs (miRNAs). We discovered that the most abundant miRNAs in MM cancer exosomes were tumor suppressors, particularly miR-16-5p. This observation lead us to hypothesize that MM cells preferentially secreted tumor-suppressor miRNAs via exosomes. Through separate avenues of potential therapeutic advance, we embarked on an innovative strategy to kill MM tumor cells. We employed small molecule inhibitors to block exosome secretion, thereby reducing miR-16-5p exosome loss and replenishing cellular miR-16-5p leading to reduced tumorigenic capacity and miR-16-5p target oncoproteins CCND1 and BCL2. Additionally, we force-fed MM tumor exosomes back to MM tumor cells, which led to cell death, and a reduction in the same oncoproteins. We recapitulated these results with direct transfection of miR-16-5p, confirmed that this is a cancer-cell specific effect, and elucidated a part of the miR-16-5p mechanism of exosome loading.

Indexed as

Gene Expression Regulation, NeoplasticAniline CompoundsAntineoplastic AgentsBenzylidene CompoundsCell DeathCell Line, TumorCell ProliferationCyclin D1ExosomesHumansIndolesLung NeoplasmsMaleimidesMesotheliomaMesothelioma, MalignantMicroRNAsAniline CompoundsAntineoplastic AgentsBCL2 protein, humanBenzylidene Compoundsbisindolylmaleimide ICCND1 protein, humanCyclin D1GW 4869IndolesMaleimidesMicroRNAsMIRN16 microRNA, humanN-alpha-benzoyl-N5-(2-chloro-1-iminoethyl)-L-ornithine amideOrnithineProto-Oncogene Proteins c-bcl-2Small Molecule Libraries

Identifiers

PMID31406207
PMCPMC6690928
OpenAlexW2969004710

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.