Chapter title |
EWS-FLI1 in Ewing's sarcoma: real targets and collateral damage.
|
---|---|
Chapter number | 4 |
Book title |
New trends in cancer for the 21st century
|
Published in |
Advances in experimental medicine and biology, December 2006
|
DOI | 10.1007/978-1-4020-5133-3_4 |
Pubmed ID | |
Book ISBNs |
978-1-4020-4966-8, 978-1-4020-5133-3
|
Authors |
Ban J, Siligan C, Kreppel M, Aryee D, Kovar H, Ban, J., Siligan, C., Kreppel, M., Aryee, D., Kovar, H. |
Abstract |
Ewing's sarcoma family of tumors (ESFT) are a clinically and scientifically very demanding group of tumors in children and young adults with still unknown histogenesis. The rate-limiting oncogenic mutation in this disease has been identified as a chromosomal translocation, t(11;22)(q24;q12), that leads to the expression of a chimeric transcription factor, EWS-FLI1. We have studied the downstream pathway of EWS-FLI1 by a dual strategy including the isolation of direct target genes from ESFT chromatin and the monitoring of transcriptomic changes after silencing of EWS-FLI1 by RNA interference. This study has lead to the identification of several directly EWS-FLI1-regulated genes and the characterization of their genomic distribution. By comparing several ESFT cell lines, not only variation in overall gene expression patterns downstream of EWS-FLIl was observed, but also differential regulation of directly EWS-FLI1-bound genes. Interestingly, there was variation between members of the same functional gene families. Studies on CD99, another diagnostic hallmark of ESFT, in relation to EWS-FLI1 provided additional evidence for context dependence of fusion protein function. Together, our study represents a first approach to the separation of essential molecular consequences from noise generated by the EWS-FLI1 gene rearrangement in ESFT. |
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