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Human Molecular Genetics Advance Access originally published online on February 23, 2006
Human Molecular Genetics 2006 15(7):1059-1070; doi:10.1093/hmg/ddl021
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© The Author 2006. Published by Oxford University Press. All rights reserved.
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed; the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact: journals.permissions@oxfordjournals.org

Schwannomin inhibits tumorigenesis through direct interaction with the eukaryotic initiation factor subunit c (eIF3c)

Daniel R. Scoles1,5,*,{dagger}, William H. Yong2,5, Yun Qin1, Kolja Wawrowsky3 and Stefan Matthias Pulst1,4,5

1Division of Neurology, CSMC Burns and Allen Research Institute, 2Department of Pathology, UCLA School of Medicine and 3Confocal Core, CSMC Burns and Allen Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA and 4Department of Neurobiology and 5Department of Medicine, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, CA 90048, USA

* To whom correspondence should be addressed at: Division of Neurology, Cedars-Sinai Medical Center, Room D-1089, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA. Tel: +1 3104232159; Fax: +1 3104239753; Email: scolesd{at}cshs.org

Received November 18, 2005; Accepted February 7, 2006

The neurofibromatosis 2 (NF2) tumor suppressor protein, schwannomin or merlin, is commonly lost upon NF2 gene mutation in benign human brain tumors. We identified the p110 subunit of the eukaryotic initiation factor 3 (eIF3c) as a schwannomin interacting protein. The eIF3 complex consists of ~10 subunits whose functions are only recently becoming known. Interaction between schwannomin and eIF3c suggests a role for schwannomin in eIF3c-mediated regulation of proliferation related to changes in protein translation. We found that schwannomin was most effective for inhibiting cellular proliferation when eIF3c was highly expressed. When we examined these proteins in 14 meningiomas, we observed high eIF3c abundance in those that had lost schwannomin expression but low eIF3c abundance in those retaining schwannomin. Consequently, eIF3c appears to be involved in NF2 pathogenesis and deserves to be investigated as a prognostic marker for NF2 and target for treatment of NF2 patient tumors.

{dagger} Present address: Women's Cancer Research Institute, Cedars-Sinai Medical Center, Room D-1089, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA.


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