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dc.contributor.author Hoda MA,
dc.contributor.author Munzker J,
dc.contributor.author Ghanim B,
dc.contributor.author Schelch K,
dc.contributor.author Klikovits T,
dc.contributor.author Laszlo, Viktoria
dc.contributor.author Sahin E
dc.contributor.author Bedeir A
dc.contributor.author Lackner A
dc.contributor.author Döme, Balázs
dc.contributor.author Setinek U
dc.contributor.author Filipits M
dc.contributor.author Eisenbauer M
dc.contributor.author Kenessey, István
dc.contributor.author Török Szilvia
dc.contributor.author Garay, Tamás
dc.contributor.author Hegedűs, Balázs
dc.contributor.author Catania A
dc.contributor.author Taghavi S
dc.contributor.author Klepetko W
dc.contributor.author Berger W
dc.contributor.author Grusch M
dc.date.accessioned 2016-11-18T11:22:39Z
dc.date.available 2016-11-18T11:22:39Z
dc.date.issued 2012
dc.identifier 84870818616
dc.identifier.citation pagination=1978-1986; journalVolume=107; journalIssueNumber=12; journalTitle=BRITISH JOURNAL OF CANCER;
dc.identifier.uri http://repo.lib.semmelweis.hu//handle/123456789/3483
dc.identifier.uri doi:10.1038/bjc.2012.519
dc.description.abstract Background:Activins 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).Methods:The 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.Results:Concomitant 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.Conclusion:Our 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.
dc.relation.ispartof urn:issn:0007-0920
dc.title Suppression of activin A signals inhibits growth of malignant pleural mesothelioma cells
dc.type Journal Article
dc.date.updated 2016-06-09T09:36:35Z
dc.language.rfc3066 en
dc.identifier.mtmt 2172184
dc.identifier.wos 000312495300010
dc.identifier.pubmed 23169291
dc.contributor.department SE/AOK/I/II. Sz. Patológiai Intézet
dc.contributor.institution Semmelweis Egyetem
dc.mtmt.swordnote PMC PMC3516694


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