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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The zyxin-related protein Thyroid Receptor Interacting Protein 6 (TRIP6) is overexpressed in Ewing's sarcoma and promotes migration, invasion and cell growth.
Biol. Cell 105, 535-547 (2013)
BACKGROUND INFORMATION: Ewing's sarcoma (ES) is the second most common bone-associated malignancy in children and is driven by the fusion oncogene EWS/FLI1 and characterized by rapid growth and early metastasis. Here, we explored the role of the Zyxin-related protein TRIP6 (thyroid receptor interacting protein 6) in ES. The Zyxin-family comprises seven homologous proteins involved in migration and proliferation of many cell types of which Zyxin has been described as a tumor suppressor in ES. RESULTS: By interrogation of published microarray data (n = 1254), we observed that of all Zyxin-proteins only TRIP6 is highly overexpressed in primary ES compared to normal tissues. Reanalysis of published EWS/FLI1 gain- and loss-of-function microarray experiments as well as chromatin-immunoprecipitation assays revealed that TRIP6 overexpression is not mediated by EWS/FLI1. Microarray and subsequent gene-set enrichment analyses of ES cells with and without RNA interference-mediated TRIP6 knockdown demonstrated that TRIP6 expression confers a pro-proliferative and pro-invasive transcriptional signature to ES cells. While short-term proliferation was not considerably affected by TRIP6 knockdown, silencing of the protein significantly reduced migration, invasion, long-term proliferation and clonogenicity of ES cells in vitro as well as tumorigenicity in vivo. CONCLUSIONS: Taken together, our data indicate that TRIP6 acts, in contrast to Zyxin, as an oncogene that partially accounts for the autonomous migratory, invasive, and proliferative properties of ES cells independent of EWS/FLI1. This article is protected by copyright. All rights reserved.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
Clonogenicity ; Ewing's Sarcoma ; Invasion ; Migration ; Trip6; Lim-domain Proteins; Gene-expression; Glucocorticoid-receptor; Repressing Signals; Nuclear Isoform; Cancer; Family; Metastasis; Adhesion; Tumors
ISSN (print) / ISBN
0248-4900
e-ISSN
1768-322X
Zeitschrift
Biology of the Cell
Quellenangaben
Band: 105,
Heft: 11,
Seiten: 535-547
Verlag
Wiley
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Pathology (PATH)