Evidence map›Paper›PMID 32555332›Full record

ArticleOncogene2020

Profiling cytotoxic microRNAs in pediatric and adult glioblastoma cells by high-content screening, identification, and validation of miR-1300.

M Boissinot, H King, M Adams, J Higgins, G Shaw, T A Ward, L P Steele, D Tams, R Morton, E Polson and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
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

21 authors at 4 institutions in 2 countries.

M BoissinotRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.ORCID http://orcid.org/0000-0002-5241-2520
H KingRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
M AdamsBioScreening Technology Group, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
J HigginsBioScreening Technology Group, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
G ShawRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
T A WardRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.ORCID http://orcid.org/0000-0003-0937-4554
L P SteeleRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
D TamsRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
R MortonRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
E PolsonStem Cells and Brain Tumour Research Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
B da SilvaStem Cells and Brain Tumour Research Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
A DroopMRC Medical Bioinformatics Centre, University of Leeds, Clarendon Way, Leeds, LS2 9NL, UK.
J L HayesRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
H MartinSchool of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, LS2 9JT, UK.ORCID http://orcid.org/0000-0002-5455-4434
P LasloMyeloid Differentiation Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
E MorrisonCell Biology Research Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
D C TomlinsonBioScreening Technology Group, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
H WurdakStem Cells and Brain Tumour Research Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
J BondBioScreening Technology Group, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK.
S E LawlerRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK. SLAWLER@bwh.harvard.edu.ORCID http://orcid.org/0000-0002-1633-2339
S C ShortRadiation Biology and Therapy Group, Leeds Institute of Medical Research, University of Leeds, St James's Hospital, Leeds, LS9 7TF, UK. S.C.Short@leeds.ac.uk.ORCID http://orcid.org/0000-0003-4423-7256
University of Leeds · GBBabraham Institute · GBBrigham and Women's Hospital · USSt James's University Hospital · GB

Funding

Medical Research Council MR/J001171/1
6 · The paper itself

Abstract

MicroRNAs play an important role in the regulation of mRNA translation and have therapeutic potential in cancer and other diseases. To profile the landscape of microRNAs with significant cytotoxicity in the context of glioblastoma (GBM), we performed a high-throughput screen in adult and pediatric GBM cells using a synthetic oligonucleotide library representing all known human microRNAs. Bioinformatics analysis was used to refine this list and the top seven microRNAs were validated in a larger panel of GBM cells using state-of-the-art in vitro assays. The cytotoxic effect of our most relevant candidate was assessed in a preclinical model. Our screen identified ~100 significantly cytotoxic microRNAs with 70% concordance between cell lines. MicroRNA-1300 (miR-1300) was the most potent and robust candidate. We observed a striking binucleated phenotype in miR-1300 transfected cells due to cytokinesis failure followed by apoptosis. This was also observed in two stem-like patient-derived cultures. We identified the physiological role of miR-1300 as a regulator of endomitosis in megakaryocyte differentiation where blockade of cytokinesis is an essential step. In GBM cells, where miR-1300 is normally not expressed, the oncogene Epithelial Cell Transforming 2 (ECT2) was validated as a direct key target. ECT2 siRNA phenocopied the effects of miR-1300, and ECT2 overexpression led to rescue of miR-1300 induced binucleation. We showed that ectopic expression of miR-1300 led to decreased tumor growth in an orthotopic GBM model. Our screen provides a resource for the neuro-oncology community and identified miR-1300 as a novel regulator of endomitosis with translatable potential for therapeutic application.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsAdultBrain NeoplasmsCell DifferentiationCell Line, TumorCell SurvivalChildGene Expression ProfilingGlioblastomaHigh-Throughput Screening AssaysHumansMegakaryocytesMicroRNAsProto-Oncogene Proteins3' Untranslated RegionsECT2 protein, humanMicroRNAsMIRN1300 microRNA, humanProto-Oncogene Proteins

Identifiers

PMID32555332
PMCPMC7378045
OpenAlexW3036079132

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.