Evidence map›Paper›PMID 23969726›Full record

ArticleBritish journal of cancer2013

MiR-17-92 and miR-221/222 cluster members target KIT and ETV1 in human gastrointestinal stromal tumours.

C M M Gits, P F van Kuijk, M B E Jonkers, A W M Boersma, W F van Ijcken, A Wozniak, R Sciot, P Rutkowski, P Schöffski, T Taguchi and 5 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.8field-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

52 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
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  6. Noncoding RNAs in Drug Resistance of Gastrointestinal Stromal Tumor.Frontiers in cell and developmental biology · 2022
    Review
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  9. Activated M1 macrophages suppress c-kit expression via TNF-α-mediated upregulation of miR-222 in Neonatal Necrotizing Enterocolitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  10. Prognostic Impact ofCancers · 2020
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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

15 authors at 5 institutions in 4 countries.

C M M GitsDepartment of Medical Oncology, Erasmus University Medical Center - Erasmus MC Cancer Institute, Dr Molewaterplein 50, 3015 GE, Rotterdam, The Netherlands.
P F van Kuijk
M B E Jonkers
A W M Boersma
W F van Ijcken
A Wozniak
R Sciot
P Rutkowski
P Schöffski
T Taguchi
R H J Mathijssen
J Verweij
S Sleijfer
M Debiec-Rychter
E A C Wiemer
Erasmus MC Cancer Institute · NLKU Leuven · BEErasmus MC · NLKōchi University · JPThe Maria Sklodowska-Curie National Research Institute of Oncology · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGastrointestinal stromal tumours (GIST) are characterised by high expression of KIT and ETV1, which cooperate in GIST oncogenesis. Our aim was to identify microRNAs that are deregulated in GIST, have a role in GIST pathogenesis, and could potentially be used as therapeutic tool.

methodsDifferentially expressed microRNAs between primary GIST (n=50) and gastrointestinal leiomyosarcomas (GI-LMS, n=10) were determined using microarrays. Selected microRNA mimics were transfected into GIST-882 and GIST-T1 cell lines to study the effects of microRNA overexpression on GIST cells. Luciferase reporter assays were used to establish regulation of target genes by selected microRNAs.

resultsMiR-17-92 and miR-221/222 cluster members were significantly (P<0.01) lower expressed in GIST vs GI-LMS and normal gastrointestinal control tissues. MiR-17/20a/222 overexpression in GIST cell lines severely inhibited cell proliferation, affected cell cycle progression, induced apoptosis and strongly downregulated protein and--to a lesser extent--mRNA levels of their predicted target genes KIT and ETV1. Luciferase reporter assays confirmed direct regulation of KIT and ETV1 by miR-222 and miR-17/20a, respectively.

conclusionMicroRNAs that may have an essential role in GIST pathogenesis were identified, in particular miR-17/20a/222 that target KIT and ETV1. Delivering these microRNAs therapeutically could hold great potential for GIST management, especially in imatinib-resistant disease.

Indexed as

AdultAgedAged, 80 and overApoptosisCarcinogenesisCell Growth ProcessesDNA-Binding ProteinsFemaleGastrointestinal Stromal TumorsHumansMaleMicroRNAsMiddle AgedMultigene FamilyProto-Oncogene Proteins c-kitTranscription FactorsDNA-Binding ProteinsETV1 protein, humanMicroRNAsProto-Oncogene Proteins c-kitTranscription Factors

Identifiers

PMID23969726
PMCPMC3776993
OpenAlexW2057735260

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.