Evidence map›Paper›PMID 25991676›Full record

ArticleOncotarget2016

Modulation of miR-21 signaling by MPS1 in human glioblastoma.

Uday B Maachani, Anita Tandle, Uma Shankavaram, Tamalee Kramp, Kevin Camphausen

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Overview upon miR-21 in lung cancer: focus on NSCLC.Cellular and molecular life sciences : CMLS · 2018
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Expression and Clinical Pathological Significance of miR-200a in Concurrent Cholangiocarcinoma Associated with Hepatolithiasis.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Article
  15. Article
  16. Article
  17. miR-125b suppresses the proliferation of hepatocellular carcinoma cells by targeting Sirtuin7.International journal of clinical and experimental medicine · 2015
    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

5 authors at 2 institutions in 1 country.

Uday B MaachaniRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Anita TandleRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Uma ShankavaramRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Tamalee KrampRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
Kevin CamphausenRadiation Oncology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, USA.
National Institutes of Health · USNational Cancer Institute · US

Funding

The Synergy Between Radiotherapy and Molecularly Targeted AgentsZIASC010373 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI CAMPHAUSEN, KEVIN · 2009 to 2025
$22.2M
6 · The paper itself

Abstract

Monopolar spindle 1 (MPS1) is an essential spindle assembly checkpoint (SAC) kinase involved in determining spindle integrity. Beyond its mitotic functions, it has been implicated in several other signaling pathways. Our earlier studies have elaborated on role of MPS1 in glioblastoma (GBM) radiosensitization. In this study using reverse phase protein arrays (RPPAs), we assessed MPS1 mediated cell signaling pathways and demonstrated that inhibiting MPS1 could upregulate the expression of the tumor suppressor PDCD4 and MSH2 genes, by down regulating micro RNA-21 (miR-21). In GBMs miR-21 expression is significantly elevated and is associated with chemo and radioresistance. Both MPS1 and miR-21 depletion suppressed GBM cell proliferation, whereas, ectopic expression of miR-21 rescued GBM cell growth from MPS1 inhibition. Further, we demonstrate that MPS1 mediates phosphorylation of SMAD3 but not SMAD2 in GBM cells; A possible mechanism behind miR-21 modulation by MPS1. Collectively, our results shed light onto an important role of MPS1 in TGF-β/SMAD signaling via miR-21 regulation. We also, show the prognostic effect of miR-21, PDCD4 and MSH2 levels to patient survival across different GBM molecular subtypes. This scenario in which miR-21 is modulated by MPS1 inhibition may be exploited as a potential target for effective GBM therapy.

Indexed as

Apoptosis Regulatory ProteinsBrain NeoplasmsCell Cycle ProteinsCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticGlioblastomaHumansMicroRNAsMutS Homolog 2 ProteinPhosphorylationProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA-Binding ProteinsRNA InterferenceSignal TransductionApoptosis Regulatory ProteinsCell Cycle ProteinsMicroRNAsMIRN21 microRNA, humanMSH2 protein, humanMutS Homolog 2 ProteinPDCD4 protein, humanProtein Serine-Threonine KinasesProtein-Tyrosine KinasesRNA-Binding ProteinsSmad3 ProteinSMAD3 protein, humanTTK protein, humanglioblastoma multiformeMiR21MPS1MSH2PDCD4TGF-β/SMAD signaling

Identifiers

PMID25991676
PMCPMC5288158
OpenAlexW1928812466

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.