Evidence map›Paper›PMID 23169291›Full record

ArticleBritish journal of cancer2012

Suppression of activin A signals inhibits growth of malignant pleural mesothelioma cells.

M A Hoda, J Münzker, B Ghanim, K Schelch, T Klikovits, V Laszlo, E Sahin, A Bedeir, A Lackner, B Dome and 12 more

Open access · hybridAbstract read
In one paragraph

Article in British journal of cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Genomics and Functional Genomics of Malignant Pleural Mesothelioma.International journal of molecular sciences · 2020
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. PKM2 and ACVR 1C are prognostic markers for poor prognosis of gallbladder cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014
    Article
  15. Article
  16. 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

22 authors at 5 institutions in 3 countries.

M A HodaDivision of Thoracic Surgery, Department of Surgery, Comprehensive Cancer Center, Medical University of Vienna, Vienna, Austria.
J Münzker
B Ghanim
K Schelch
T Klikovits
V Laszlo
E Sahin
A Bedeir
A Lackner
B Dome
U Setinek
M Filipits
M Eisenbauer
I Kenessey
S Török
T Garay
B Hegedus
A Catania
S Taghavi
W Klepetko
W Berger
M Grusch
Comprehensive Cancer Center Vienna · ATSemmelweis University · HUOrszágos Korányi Tbc és Pulmonológiai Intézet · HUOspedale Maggiore · ITOtto Wagner Hospital · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivins control the growth of several tumour types including thoracic malignancies. In the present study, we investigated their expression and function in malignant pleural mesothelioma (MPM).

methodsThe expression of activins and activin receptors was analysed by quantitative PCR in a panel of MPM cell lines. Activin A expression was further analysed by immunohistochemistry in MPM tissue specimens (N=53). Subsequently, MPM cells were treated with activin A, activin receptor inhibitors or activin-targeting siRNA and the impact on cell viability, proliferation, migration and signalling was assessed.

resultsConcomitant expression of activin subunits and receptors was found in all cell lines, and activin A was overexpressed in most cell lines compared with non-malignant mesothelial cells. Similarly, immunohistochemistry demonstrated intense staining of tumour cells for activin A in a subset of patients. Treatment with activin A induced SMAD2 phosphorylation and stimulated clonogenic growth of mesothelioma cells. In contrast, treatment with kinase inhibitors of activin receptors (SB-431542, A-8301) inhibited MPM cell viability, clonogenicity and migration. Silencing of activin A expression by siRNA oligonucleotides further confirmed these results and led to reduced cyclin D1/3 expression.

conclusionOur study suggests that activin A contributes to the malignant phenotype of MPM cells via regulation of cyclin D and may represent a valuable candidate for therapeutic interference.

Indexed as

ActivinsAntineoplastic AgentsBlotting, WesternCell MovementCell ProliferationCell SurvivalCyclin DGene Expression Regulation, NeoplasticGene SilencingHumansImmunohistochemistryMesotheliomaPhenotypePhosphorylationPleural NeoplasmsReal-Time Polymerase Chain Reactionactivin AActivinsAntineoplastic AgentsCyclin DRNA, Small InterferingSmad2 ProteinSMAD2 protein, human

Identifiers

PMID23169291
PMCPMC3516694
OpenAlexW1980771329

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.