MiR-200a-mediated suppression of non-muscle heavy chain IIb inhibits meningioma cell migration and tumor growth in vivo

O. Senol, T. B.M. Schaaij-Visser, E. P. Erkan, C. Dorfer, G. Lewandrowski, T. V. Pham, S. R. Piersma, S. M. Peerdeman, T. Ströbel, B. Tannous, N. Saydam, I. Slavc, E. Knosp, C. R. Jimenez, O. Saydam

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

miR-200a has been implicated in the pathogenesis of meningiomas, one of the most common central nervous system tumors in humans. To identify how miR-200a contributes to meningioma pathogenesis at the molecular level, we used a comparative protein profiling approach using Gel-nanoLC-MS/MS and identified approximately 130 dysregulated proteins in miR-200a-overexpressing meningioma cells. Following the bioinformatic analysis to identify potential genes targeted by miR-200a, we focused on the non-muscle heavy chain IIb (NMHCIIb), and showed that miR-200a directly targeted NMHCIIb. Considering the key roles of NMHCIIb in cell division and cell migration, we aimed to identify whether miR-200a regulated these processes through NMHCIIb. We found that NMHCIIb overexpression partially rescued miR-200a-mediated inhibition of cell migration, as well as cell growth in vitro and in vivo. Moreover, siRNA-mediated silencing of NMHCIIb expression resulted in a similar migration phenotype in these cells and inhibited meningioma tumor growth in mice. Taken together, these results suggest that NMHCIIb might serve as a novel therapeutic target in meningiomas.

Original languageEnglish (US)
Pages (from-to)1790-1798
Number of pages9
JournalOncogene
Volume34
Issue number14
DOIs
StatePublished - May 26 2014
Externally publishedYes

Bibliographical note

Funding Information:
Support for this work was provided, in part, by Forschungsgesellschaft for Brain Tumors (to OS, NS), EU-FP7-PEOPLE-2011-CIG (to OS) and Association for Conduct of Scientific Research in the Field of Neonatology and Pediatric Intensive Care: ‘Unser Kind’ (to OS). We thank Dr Marianne F James for providing us with AC030 cells.

Publisher Copyright:
© 2015 Macmillan Publishers Limited.

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