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* Ihre Aktion:   suchen [und] (PICA Prod.-Nr. [PPN]) 1662806620
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Online-Artikel
 
K10plusPPN: 
1662806620     Zitierlink
Aufsatz: 
Pleiotropic effects of miR-183~96~182 converge to regulate cell survival, proliferation and migration in medulloblastoma / Shyamal Dilhan Weeraratne, Vladimir Amani, Natalia Teider, Jessica Pierre-Francois, Dominic Winter, Min Jeong Kye, Soma Sengupta, Tenley Archer, Marc Remke, Alfa H.C. Bai, Peter Warren, Stefan M. Pfister, Judith A.J. Steen, Scott L. Pomeroy, Yoon-Jae Cho
Autorin/Autor: 
Weeraratne, Shyamal Dilhan [Verfasserin/Verfasser] info info
Beteiligt: 
Remke, Marc, 1981- [Verfasserin/Verfasser] info info ; Pfister, Stefan, 1974- [Verfasserin/Verfasser] info info
Enthalten in: 
Acta neuropathologica. - Berlin, Heidelberg : Springer, 1961-. - Bd. 123 (2012), 4, S. 539-552 = 14 S.
Sprache(n): 
Englisch
Anmerkung: 
Gesehen am 04.04.2019


Link zum Volltext: 
Digital Object Identifier (DOI): 10.1007/s00401-012-0969-5


Sonstige Schlagwörter: 
Inhaltliche
Zusammenfassung: 
Medulloblastomas are the most common malignant brain tumors in children. Several large-scale genomic studies have detailed their heterogeneity, defining multiple subtypes with unique molecular profiles and clinical behavior. Increased expression of the miR-183~96~182 cluster of microRNAs has been noted in several subgroups, including the most clinically aggressive subgroup associated with genetic amplification of MYC. To understand the contribution of miR-183~96~182 to the pathogenesis of this aggressive subtype of medulloblastoma, we analyzed global gene expression and proteomic changes that occur upon modulation of miRNAs in this cluster individually and as a group in MYC-amplified medulloblastoma cells. Knockdown of the full miR-183~96~182 cluster results in enrichment of genes associated with apoptosis and dysregulation of the PI3K/AKT/mTOR signaling axis. Conversely, there is a relative enrichment of pathways associated with migration, metastasis and epithelial to mesenchymal transition, as well as pathways associated with dysfunction of DNA repair in cells with preserved miR-183 cluster expression. Immunocytochemistry and FACS analysis confirm induction of apoptosis upon knockdown of the miR-183 cluster. Importantly, cell-based migration and invasion assays verify the positive regulation of cell motility/migration by the miR-183 cluster, which is largely mediated by miR-182. We show that the effects on cell migration induced by the miR-183 cluster are coupled to the PI3K/AKT/mTOR pathway through differential regulation of AKT1 and AKT2 isoforms. Furthermore, we show that rapamycin inhibits cell motility/migration in medulloblastoma cells and phenocopies miR-183 cluster knockdown. Thus, the miR-183 cluster regulates multiple biological programs that converge to support the maintenance and metastatic potential of medulloblastoma.
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